MS news and research
This page documents breaking multiple sclerosis news and research stories as they occur during the month.
For news and research for the previous 12 months please use the links on the menu on the left.
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‘Four out of five misdiagnosed’
Four out of five people with multiple sclerosis are misdiagnosed, a charity has warned.
The MS Society said 25 per cent of people with MS are told they have a trapped nerve, while about two-fifths (39 per cent) are left waiting a year or more before they are diagnosed.
The charity said that while MS can be difficult to diagnose, delays such as these can be harmful as they prevent people from taking the necessary steps to manage their condition effectively.
Michelle Mitchell, chief executive at the MS Society, said: "Our findings highlight the struggle people go through for years before they get an MS diagnosis.
"Being misdiagnosed or experiencing symptoms that can't be explained can put a considerable strain on people's emotions and health."
There are more than 100,000 people living with the condition in the UK and 5,000 new cases are diagnosed every year.
"It's disappointing," said Dr Alan Thompson, consultant neurologist at the National Hospital for Neurology in London.
"One of the main reasons is that the symptoms of MS are variable and could be caused by a lot of other things.
"It can be a mixture of numbness and tingling or a bit of imbalance or a loss of vision and these symptoms can last for four to six weeks and then disappear.
"There's a general lack of awareness of MS and what the symptoms are and this is what we need to address."
Of the 1,515 people questioned for the survey to mark World MS Day, the most common early symptoms were reported as being numbness and altered sensations in different parts of the body (53 per cent), sight problems (47 per cent) and difficulty with walking (41 per cent).
Source: Sky News © 2015 Sky UK (27/05/15)
Patients in Northern Ireland with multiple sclerosis are being told by text message that they have the condition, it has been claimed.
And one GP in Antrim has hit out at waiting times, with some patients waiting for up to a year to see a neurologist.
One MS patient said: “I have spoken to people who were told they had MS by text message.
“It isn’t standard practice although I’m aware of it happening on a number of occasions which makes you wonder how many people it has happened to.
“It’s such a devastating thing to hear that you have MS and there are definitely better ways to get the diagnosis.
“My own consultant was very matter of fact when he told me, he didn’t sugar coat it, there was definitely no hand holding or hugs but it was better than being told by text message.
“There are a lot of things you have to get your head around when you get the news.
“When I was told I had MS, I had visions of spending the rest of my life in a wheelchair and I went in to a really deep depression for a couple of years.”
There are an estimated 4,500 people in Northern Ireland with MS, with 200 new cases being diagnosed every year.
Meanwhile, an Antrim-based GP has hit out at waiting times for hospital appointments with neurologists.
Dr Allen McCullough said: “Referral times for neurology are off the scale.
“Review appointments are currently running one year behind and any patient I have referred in the past two years has gone privately initially to get seen and get a diagnosis.
“The situation with review appointments is so bad we are being told to refer existing neurology patients, who have been diagnosed with a neurological condition and therefore we know they need to be seen, as new patients.”
Source: Belfast Live © MGN 2015 (27/05/15)
MS patient summit hailed a success(27/05/15)
A patient summit for people with MS held in Rome has been hailed a success by organisors.
Reaching 8.5 million people around the world, the social media response also saw the summit became a trending topic on Twitter with #thinkMS surging to become the top healthcare hashtag on Friday.
MS campaigner Kaz Aston, who has diagnosed with MS at the age of 21, chaired and moderated the event.
She said: "The 2015 patient summit was excellent. The focus was all about MS patients and how to best link patient expertise to progress, research, care and community services.
"Sustainable ways to improve MS treatment, the sharing of information with the aid of modern technology such as social media... Everything was up for discussion."
An estimated 2.5 million people around the world have MS. Most are diagnosed between the ages of 20 to 40, and Approximately three times as many women have been diagnosed as men.
"The expert patient discussions were amazing and identified the key resources needed to champion the best practices, to implement new education solutions and to be pro-active in developing common and consistent language at both local and international levels," said Miss Aston.
Key speakers included Dr Vittorio Martinelli, Aliki Vrienniou, Mary Baker, Jean Hardiman-Smith and Sir Nick Partridge (UK).
Breakout groups focused their discussions on three key areas: Patient rights, the development of health care services and positioning patients as experts.
A number of international charities and organizations were also in attendance.
"The 2015 World MS Patient Summit uncovered what it can really mean to make decisions about MS research, treatment, care and the lifestyle options available if you're a patient,” said Miss Aston.
“People can navigate their way through changing the current healthcare landscapes to positively influence and campaign for long-term change and improvement."
Source: The Huffington Post Copyright ©2015 TheHuffingtonPost.com, Inc (27/05/15)
Exploratory research conducted at Virginia Commonwealth University and the University of Illinois at Chicago may translate into a new therapeutic agent to treat progressive multiple sclerosis, reports Multiple Sclerosis News Today.
Researchers in the laboratories of Dr Jefferey L. Dupree and Dr Douglas L. Feinstein tested a new compound in mice with induced multiple sclerosis and found the compound reduced neurodegeneration and helped improve symptoms.
The compound, lanthionine ketimine, is a naturally occurring molecule that binds to collapsin response mediator protein-2 (CRMP2), which is a protein found in the brain that helps regulate vital neuronal activities. In order to use this compound to treat mice with induced multiple sclerosis, the researchers needed to chemically modify it into a cell-permeable state. The resulting molecule was lanthionine ketimine ethyl-ester (LKE), which was shown to promote neurogenesis and healthy nervous system function.
As explained in the journal article, “Lanthionine Ketimine Ester Provides Benefit in a Mouse Model of Multiple Sclerosis,” which was published in Journal of Neurochemistry, the authors induced multiple sclerosis in mice using the well-accepted model of experimental autoimmune encephalomyelitis (EAE). After mice began to show moderate clinical symptoms of multiple sclerosis, the researchers mixed LKE into the animals’ food so that mice were treated whenever they decided to eat.
After four weeks of ingesting LKE, mice had lower levels of inflammation than those that did not receive LKE but were induced with EAE. LKE-treated mice also showed lower degeneration of the optic nerve and spinal cord, showing only minimal damage to the myelin sheath around the axons. The protective effect was more pronounced in the optic nerve, but the spinal cord also showed great benefit from LKE treatment.
If the researchers continue to pursue LKE and design a well-controlled dosing study in other animal models of multiple sclerosis, the compound may be a potential candidate for clinical trials in patients with progressive multiple sclerosis.
“Only few drugs have been shown to reduce neurodegeneration in multiple sclerosis,” stated the authors. By identifying neuronal protection in the spinal cord and optic nerve, the researchers showed that LKE is a novel and strong candidate for testing in progressive multiple sclerosis.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (26/05/15)
A new kind of brain implant senses a patient's intent to move a robotic arm, offering new promise to people who are paralyzed or have lost limbs, researchers claim.
Erik Sorto, 34, is "the first person in the world to have a neural prosthetic device implanted in a region of the brain where intentions are made," said the study in the journal Science.
Sorto, who was paralysed from the neck down at age 21 after a gunshot wound, can now make a hand-shaking gesture, grab a cup to drink from and even play "rock, paper, scissors" with his robotic arm.
Previous attempts to use brain implants to control prosthetics have been placed in the motor cortex, which controls motion.
This experiment was done by placing two micro-electrode arrays in the posterior parietal cortex, or PPC. This part of the brain processes plans for movements including reach and grasp.
"When you move your arm, you really don't think about which muscles to activate and the details of the movement -- such as lift the arm, extend the arm, grasp the cup, close the hand around the cup, and so on," said principal investigator Richard Andersen, professor of neuroscience at Caltech.
"Instead, you think about the goal of the movement, for example, 'I want to pick up that cup of water.' So in this trial, we were successfully able to decode these actual intents, by asking the subject to simply imagine the movement as a whole, rather than breaking it down into a myriad of components."
The result is a more fluid movement than the jerky kind of motions seen in previous experiments, scientists said.
Sorto received the brain implant in 2013 and has been practicing with it at Rancho Los Amigos National Rehabilitation Centre ever since, learning to control a robotic arm that is not attached to his body.
He was able to control the arm in his very first attempt, about two weeks after his brain surgery.
Video images released by the science team show Sorto controlling a computer cursor, drinking a beverage and making a hand-shaking gesture with the arm.
"I was surprised at how easy it was," said Sorto, a single father of two.
"I joke around with the guys that I want to be able to drink my own beer - to be able to take a drink at my own pace, when I want to take a sip out of my beer and to not have to ask somebody to give it to me. I really miss that independence," he added.
"I think that if it were safe enough, I would really enjoy grooming myself - shaving, brushing my own teeth. That would be fantastic."
The clinical trial was a collaboration between Caltech, the Keck School of Medicine of the University of Southern California (USC) and Rancho Los Amigos National Rehabilitation Centre.
"These very important early clinical trials could provide hope for patients with all sorts of neurologic problems that involve paralysis such as stroke, brain injury, ALS and even multiple sclerosis," said co-author Christianne Heck, associate professor of neurology at USC.
Source: The Daily Mail © Associated Newspapers Ltd 2015 (22/05/15)
If you already claim Disability Living Allowance (DLA), from 25 May 2015 if you live in the postcode areas for Bristol, Cambridge, Colchester, Dartford, Gloucester, Milton Keynes, Paisley, Romford Swindon, Spalding or Southend you will be asked to claim ‘Personal Independence Payment’ instead.
You may need support to fill in the forms and prepare for your face-to-face assessment with an independent health professional. You can get in touch with the MS-UK Helpline and talk to one of our MS Advisors who have all received welfare rights training and will be able to support you though the process.
We’re here to help
The MS-UK Helpline is open Monday to Friday, 9am to 5pm each day.
• Call for free on 0800 783 0518 (Call charges apply from a mobile)
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• Send us an e-mail to email@example.com
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Source: MS-UK (22/05/15)
Results from the BENEFIT11 trial has found that early treatment with IFNB-1b leads to improvements in cognition and fatigue in the long-term, as well as sustained employment and favourable magnetic resonance imaging (MRI) outcomes, measured at the 11-year mark, according to the study Long-Term Impact Of Early MS Treatment With Interferon Beta-1b: Clinical, MRI, Employment And Patient-Reported Outcomes (PROs) at the 11-Year Follow-up of BENEFIT (BENEFIT 11).
The BENEFIT trial included patients with MS and clinically isolated syndrome. Clinically isolated syndrome consists of an initial attack on myelin in the central nervous system, putting someone at risk for developing MS.
People who participated in the BENEFIT study either received IFNB-1b or a placebo (sugar pill). After the second case of clinically isolated syndrome, or after two years, all participants in the study were given IFNB-1b. The researchers measured MRI, performed laboratory tests, and took measurements about other outcomes eleven years after the beginning of the study.
278 MS patients participated in the study. At year 11, those who had received IFNB-1b still had a lower overall yearly relapse rate and a longer time to their first MS relapse than people who received placebo. They also had a lower incidence of clearly diagnosed MS. The expanded disability status scale (EDSS) score — a measurement of impairment used in people with MS — was the same in both groups. The paced auditory serial addition test (PASAT) scores, a measurement of cognitive ability, were high in both groups. Of the 81% who were employed when their physician first diagnosed their clinically isolated syndrome, 73 per cent were still employed.
A total of 12 per cent had retired early or were receiving long-term disability, as opposed to 2.9 per cent at the beginning of the study. Furthermore, 64 per cent did not take any sick leave for the most recent year. Health-related quality of life did not change. A total of 46 per cent of study subjects experienced no fatigue. Both groups had similar MRIs. A total of 86 per cent had no gadolinium-enhancing lesions, indicators of areas in which myelin is damaged.
In their report, the researchers concluded that “results from BENEFIT11 support a long-term impact of early treatment with IFNB-1b on clinical measures, including cognition and fatigue, and health economic and MRI outcomes.”
Source: Multiple Sclerosis News Today © BioNews Services 2015 (21/05/15)
New research into the causes of the excessive inflammation that drives multiple sclerosis has identified a faulty "brake" within immune cells, a brake that should be controlling the inflammation. This points to a potential target for developing new therapies to treat MS and could have important implications for other autoimmune diseases, such as the colon disease colitis and the chronic skin condition atopic dermatitis, say researchers.
Further, the work has produced new research models of MS symptoms such as movement disorders and balance control problems that have, until now, resisted efforts to mimic them effectively in the lab. These models represent important new tools in the efforts to better understand - and eventually cure - MS and other autoimmune conditions.
The researchers determined that a mutation in the gene Nlrp12 was causing immune cells known as T cells to go haywire. Normally, the researchers determined, the protein the gene produces acts as a brake within T cells to control the inflammatory response. But a mutation in that gene disrupts the natural process and provokes severe inflammation - with effects the researchers found most intriguing.
To the researchers' surprise, the resulting inflammation did not produce the paralysis often associated with MS. It did, however, produce other MS symptoms - such as movement disorders and problems with balance control - which scientists have struggled to replicate in experimental lab settings.
"It's important to note that MS is a spectrum disorder - some patients present with paralysing conditions and some patients don't," said researcher John Lukens, PhD, of the University of Virginia School of Medicine Department of Neuroscience and its Center for Brain Immunology and Glia. "Not everybody's symptoms are the same, so this might give us a glimpse into the etiology or pathogenesis of that family of MS."
By blocking the inflammatory response, doctors may one day be able to control the symptoms it causes, both in MS and in other diseases driven by hyperinflammation.
The findings have been published by the scientific journal Immunity. Source: Science Newsline (20/05/15)
A drug that could halt the progression of MS may soon be developed thanks to a discovery by a team at the CHUM Research Centre and the University of Montreal.
The researchers have identified a molecule called MCAM, and they have shown that blocking this molecule could delay the onset of the disease and significantly slow its progression. These encouraging results from in vitro tests in humans and in vivo tests in mice have been published in the Annals of Neurology. "We believe we have identified the first therapy that will impact the quality of life of people with MS by significantly reducing the disability and the disease's progression," said Dr. Alexandre Prat, lead author of the study, researcher at the CRCHUM, and professor in the Department of Neurosciences at the University of Montreal.
The brain is normally protected from attacks by the blood-brain barrier. The blood-brain barrier prevents immune cells - lymphocytes - from entering the central nervous system. In people with MS, there is often leakage. Two types of lymphocytes, CD4 and CD8, find a way to cross this protective barrier. They attack the brain by destroying the myelin sheath that protects neurons, resulting in decreased transmission of nerve impulses, and plaque formation.
In 2008, Dr. Prat's team identified a cell adhesion molecule, called MCAM (Melanoma Cell Adhesion Molecule), which plays a crucial role in dysregulation of the immune system observed in MS.
"Our studies have shown that MCAM is necessary for the migration of CD4 and CD8 across the blood-brain barrier. If we block the interaction of MCAM with the protein to which it normally binds, we decrease the disease's activity," he said.
Independently, the biotechnology company Prothena Corporation plc also discovered complementary data regarding MCAM, which led to an ongoing collaboration between the CRCHUM and Prothena.
"We observed a decrease of approximately 50 per cent of the condition in mice with experimental autoimmune encephalomyelitis (EAE), the most widely used animal model of MS. What is especially significant is that we can stop it from the first symptoms in addition to having an impact on its progression, which is a first," noted Prat.
MS develops in most patients in two phases. For 10 to 15 years, there are outbreaks of symptoms interspersed with remissions. Later, the diseases progresses and the disability worsens, leading to the use of a cane or wheelchair. Currently, none of the drugs available on the market affect progression.
Prothena has developed a potentially disease-modifying antibody, called PRX003, which is designed, to inhibit MCAM function and thus prevent migration of destructive lymphocytes into tissue. Prothena expects to initiate clinical trials of PRX003 in healthy volunteers by the end of June, and anticipates a study in patients with psoriasis in 2016. Beyond psoriasis, anti-MCAM antibodies may be useful for treating a variety of diseases, including progressive forms of multiple sclerosis.
Source: EurekaAlert! Copyright © 2015 by the American Association for the Advancement of Science (AAAS) (20/05/15)
Genzyme and Ablynx form MS pact(18/05/15)
Sanofi group Genzyme and Belgian biotech Ablynx have formed a pact to investigate the latter’s nanobodies against a target that plays an important role in MS, in the hope of targeting the neurodegeneration linked with the condition.
Under the research deal, Genzyme has bought itself the right to perform in vitro and in vivo research with Ablynx’s Nanobodies in MS-relevant models in return for an undisclosed exclusivity fee. When these studies are complete, Genzyme has the option of negotiating a license agreement.
Ablynx has already generated “potent” Nanobodies against the Genzyme’s target of interest and confirmed their activity in preclinical models, the firm noted.
Commenting on the move, Johanne Kaplan, who heads up Neuroimmunology Research at Genzyme, said the project supports its research “that includes the exploration of novel therapeutic platforms to address unmet needs in multiple sclerosis”.
Further terms of the deal were not released.
Source: PharmaTimes Copyright PharmaTimes 2015 (18/05/15)
New insights into MS treatment(18/05/15)
Data from two Novartis phase III clinical trials show that adding brain shrinkage (brain volume loss) to an existing tool to assess multiple sclerosis activity (m-Rio) will give a more precise prediction of the likelihood of future disability progression.
A pooled analysis from the two-year Freedoms and Freedoms II trials also further confirm the high efficacy of Fingolimod in previously treated patients with highly-active relapsing MS. In the trials, patients on Fingolimod achieved no evidence of disease activity (Neda) across four key measures: relapses, MRI lesions, brain shrinkage and disability progression. Achieving Neda is especially critical for highly-active RMS patients, who are likely to lose more physical and cognitive functions over time despite being treated.
The Fingolimod clinical trial data was presented at the 67th American Academy of Neurology annual meeting in Washington, DC. Developed by Novartis, Fingolimod is the only oral disease-modifying therapy to impact the course of relapsing MS with high efficacy across four key measures of disease activity: relapses, MRI lesions, brain shrinkage (brain volume loss) and disability progression.
“Accurate assessment of disease activity is key to guide treatment decisions in relapsing MS. These data on Fingolimod and new methods of assessing the impact of MS have the potential to give physicians a more comprehensive picture of an individual’s disease and allow patients to better understand their MS,” said Dr Ludwig F. Damian, consultant neurologist.
“Novartis is committed to innovation beyond the research and development of new treatments to help physicians and patients improve how MS is managed,” said Dr Nikolaos Tripodis, Novartis Healthcare Philippines president and managing director.
Source: INQUIRER.net © Copyright 1997-2015 INQUIRER.net (18/05/15)
Gut bacteria could hold key(18/05/15)
Gut bacteria could hold the key to treating conditions including multiple sclerosis, Parkinson’s and mental illness, scientists have said.
The trillions of intestinal bacteria affect every aspect of our health and the way we behave, say researchers.
Professor Simon Carding, who runs the gut health programme at the Institute of Food Research, said: “The human gut is the inner tube of life.
"It is home to hundreds of trillions of microorganisms.
"They outnumber the cells that make up the body by more than 10-to-one, but far from doing us harm, they are working to keep us healthy.”
Researchers say eating a varied diet makes the microbes more diverse and improves health.
But the intake of healthy bacteria has declined as people eat more processed food such as pizzas, pies and cereals.
Professor Carding, of East Anglia University, said: “Such changes are increasingly being associated with a number of chronic diseases including those that affect the brain.”
But by studying patients’ intestines doctors may be able to create tailored treatments, he said.
Scientists are working on moving healthy bacteria from a donor to a sick patient.
Recent studies show those with potentially deadly C-diff bacteria can be cured by such transplants.
Professor Carding believes many other conditions may be “improved or even eliminated” by the same bacterial transfer.
A new book, The Diet Myth, claims fast food kills off microbes that help us stay slim.
Author Tim Spector, professor of genetic epidemiology at King’s College London, says this partly explains rising obesity levels.
Source: Daily Express Copyright ©2015 Northern and Shell Media Publications (18/05/15)
Researchers solve MS ‘puzzle’(18/05/15)
Evidence has long suggested multiple sclerosis is an autoimmune disease, but researchers have been puzzled because they found the same T cells that attack the myelin sheathing around nerve cells in MS patients are present in healthy subjects as well.
Now researchers from the Yale School of Medicine and colleagues at the Massachusetts Institute of Technology (MIT) report that auto-reactive T cells in MS patients produce different types of inflammatory hormones called cytokines than they do in healthy subjects.
“In most people, these T cells are acting to repair tissue, but in MS patients, they do damage to the nervous system,” said Dr. David Hafler, the William S. and Lois Stiles Edgerly Professor of Neurology and senior author of the study, published May 14 in the journal Science Translational Medicine.
The Yale-led team analysed T cell populations from 23 MS patients and 22 healthy controls. Existing drugs target the MS-specific cytokines identified in the study and should be a promising new treatment for the disease, the authors say.
Hafler also noted the same sort of process might be found in other autoimmune diseases, such as rheumatoid arthritis and Type 1 diabetes.
Yonghao Cao of Yale and Brittany A. Goods of MIT are co-first authors of the paper.
The research was funded by the National Institutes of Health and the National Multiple Sclerosis Society.
Source: Bioscience Technology © Copyright 2015 Advantage Business Media (18/05/15)
Gene linked to interferon-beta treatment(18/05/15)
A new study led by investigators at Brigham and Womens Hospital (BWH) reports the discovery of a genetic variant associated with a patients likelihood of responding to interferon-beta, one of the medications used in treating multiple sclerosis.
Published in the Annals of Neurology, the study also presents evidence that the affected gene, SLC9A9, may have a broader role in regulating the development and activity of certain immune cells that play important roles in inflammatory diseases like MS.
The variant most predictive of whether or not a patient would respond to the drug was found in the gene SLC9A9.
"This study highlights the fact that genetic variation has a role in the course of a patient's MS, but that this role is modest and will require much larger studies to be understood in detail," said Philip De Jager, MD, PhD, who directs the Program in Translational NeuroPsychiatric Genomics at the Ann Romney Center for Neurologic Diseases at BWH.
A large, ongoing study of MS patients called CLIMB, based out of the Partners Multiple Sclerosis Center, was integral to the current work and will continue to follow patients over the course of treatment to identify predictors of future disease course and the effectiveness of treatments.
Additional support was provided by the National MS Society, Fondazione Italiana Sclerosi, the French MS society Association pour la recherche sur la sclerose en plaques, the Club francophone de la SEP, and the Reseau francais pour la genetique de la SEP.
De Jager is a recipient of the prestigious Harry Weaver Neuroscience Scholar of the National MS Society.
Source: Demanjo Copyright © Demanjo 2015 (18/05/15)
A long-term study following multiple sclerosis (MS) patients taking interferon beta-1b, suggests the earlier therapy is started, the greater the benefit.
The results of the BENEFIT 11 study were published last week in Neurology.
In MS, the immune system mistakenly sees myelin, the protective covering of nerve cells, as an enemy to be destroyed. When a person has an MS attack the nerves are damaged and can result in a whole slate of symptoms that depend on the location of the inflammation.
The symptoms can be mild or dramatic. They can range from numbness and tingling to paralysis, cognitive issues, bowel and bladder problems, and even blindness.
Starting Early Is Key
For this study, researchers examined people who had suffered from clinically isolated syndrome (CIS), which is a singular neurological event resulting in symptoms similar to those seen in MS.
While the patients may appear to have the disease, doctors cannot give a definite diagnosis until after a person has at least two attacks. Each attack must result in lesions, or patches of inflammation, in different spots on the brain or spinal cord. Patients who have CIS have yet to meet this requirement and not all of them will go on to be diagnosed with MS.
Many will, however, so CIS is seen as a possible precursor to MS. By including these patients in this study, researchers were trying to catch MS in its earliest stage to see if treating with interferon beta-1b before the disease had time to do damage could make a difference in long-term outcomes.
Over the Long Haul
The original study randomly assigned participants to receive either interferon beta-1b or a placebo. After either a second neurological event or two years, all patients were given interferon beta-1b.
Researchers followed 278 patients over an 11-year period and found that people with CIS who received interferon beta-1b had a lower relapse rate and a longer time from first episode to receiving a definite MS diagnosis.
Early in relapsing MS, the body has the ability to heal damaged myelin to near perfect condition. Because of this, symptoms a patient suffers during an attack may disappear after the episode is over. But scar tissue accumulates over time. This scar tissue does not transmit nerve impulses as effectively as the original myelin. As a result, symptoms can remain and disability can accumulate.
For that reason, beginning treatment early — and taking it as prescribed — is crucial.
There are currently 12 disease-modifying therapies (DMTs) approved by the Food and Drug Administration (FDA) to treat MS. Each of these medications comes with possible side effects and varying levels of effectiveness.
According to a consensus paper published by the Multiple Sclerosis Coalition, “Early successful control of disease activity — including the reduction of clinical and sub-clinical attacks and the delay of the progressive phase of the disease — appears to play a key role in preventing accumulation of disability, prolonging the ability of people with MS to remain active and engaged, and protecting quality of life.”
Interferon beta-1b came on the market in 1993 as the first FDA-approved DMT for MS. It has been sold under the brand name Betaseron since that time. In 2014, the drug got a makeover. This version of the drug, called Extavia, only has to be injected twice a month.
Source: HealthlineNews Copyright © 2005 - 2015 Healthline Networks, Inc (15/05/15)
British expertise will be leading the way at the International MS Patient Summit to be held in Rome on 22 May. And patients’ own expertise will be top of the conference agenda. MS campaigner Kaz Aston has been named as conference moderator, and three of the five speakers will be from the United Kingdom.
Emphasis of the Rome conference will be on MS patients and the expertise that they can bring to treating the condition.
“This event is different,” says Kaz Aston, “because it’s all about the patient, and about the ‘expert patient’ as a concept - recognising that MS patients have a lot to bring to the table.
“Because MS patients include many younger people, they tend to be quite active, and keen to talk and share, especially over social media. So there’s a lot of new ideas coming out about patients taking some responsibilities for themselves. This conference is all about the role of the patient in treatment.”
The conference will be attended by charities and organisations providing support for people affected by MS from around the world. Aim of the summit is to share the latest research findings, and strategies to support patients with information and treatments that delegates can take back to their countries. Some of the delegates attending will themselves have MS.
Kas believes there is a strong sense of community among people with MS and a willingness to come together to help each other, rather than relying solely on the medical community for treatment.
“People are keen to know, to share and to exchange stories and experiences about what works for them,” she says.
“And it’s not always about trying to treat the MS directly, it can also be about the things that MS generates in your life - so there are work and lifestyle issues as well which people with MS want to talk about.
“Even something as simple as changes in weather can affect people - increases in temperature can cause a lot of extra problems which can be alleviated if you anticipate them and know how best to respond.”
Currently there are a range of treatments including both pharmaceutical and non-pharmaceutical therapies, but because the precise cause of MS remains unknown, treatment is to some extent experimental. There are dietary supplements that are being tried and also anti-oxidants, which seem to be promising.
Kaz says: “Rome will be about engaging with people with MS, to help develop support services for them. Some events like this can be a little academic - but what people suffering from MS want to know is: what does this mean for me? Our hope is that the conference will bring greater clarity and greater involvement for patients.
“I have lived with MS for the last 22 years and, although I’ve had to battle my way through some tough attacks in the past, I’m always inspired by the experiences I’ve had and the people I’ve met along the way. Over the last couple of years, I’ve developed a real passion for drag racing, sailing, radio & golf – and it helps me to raise awareness for MS as well as being a great way of fundraising and spreading the word about the condition and how it can be tackled.”
Source: SourceWire © 1997-2015 DWPub (15/05/15)
A team of Canadian scientists has found a way to break the barrier of the human body that keeps the nervous and circulatory systems apart, and inject the drugs directly into the brain using “carrier” antibodies.
That system known as the blood-brain barrier (BBB) protects the human skull from any microbes or chemicals, thus keeping the brain clean.
But this barrier also filters good things, such as disease fighting drugs from entering the nervous system. It only allows a selected few types of molecules to cross including water, some gases and lipid soluble molecules.
Scientists from the Canadian National Research Council have been battling for years to find a way to trick it and get the drugs to where they are most needed - to the human brain.
Currently, researchers say they have found a way based on the so-called “single domain antibodies” (SDA). It includes using special molecular fragments that are capable of tricking the blood-brain barrier (BBB) and making it believe they should be let through to the brain. The antibodies are able to squeeze past the barrier not just because of their size (these are fragments that consist of one molecule) but also due to being familiar to some of the receptors along the blood-brain barrier.
The single domain antibodies are exploiting the same mechanism that allows nutrients into the brain, and are able to bind chemically to other molecules.
The scientists add that the method allows them to target multiple types of diseases by producing different carrier molecules.
The method is part of the NRC's Therapeutics Beyond Brain Barriers (TBBB) program, which has been developing special carrier molecules for the past six years.
"It really opens the possibilities to use many different types of therapeutics for different diseases that we couldn't really use before unless we inject them directly into the brain which is highly invasive,” Dr. Danica Stanimirovic, the project`s scientific head,said.
Scientists add that it could become a significant step towards slowing the spread of brain diseases like Alzheimer’s, multiple sclerosis and Parkinson’s.
The discovery follows years of scientific work. At the moment drugs are usually placed into the blood and there they find a way around the body.
Still, researchers say it will take over a decade to finalise clinical trials.
Source: RT © Autonomous Nonprofit Organization “TV-Novosti”, 2005–2015. (15/05/15)
When the seasons change, your immune system response may also change, researchers report.
These findings might explain why conditions such as rheumatoid arthritis and heart disease are worse in the winter than in the summer, the new study finds.
The researchers from the University of Cambridge analysed genes from more than 16,000 people worldwide, including those from both the Northern and Southern hemispheres. They found that the activity of nearly one-quarter of the genes differed according to the time of the year. Some are more active in winter and some are more active in summer, the research revealed.
Seasons also affect our immune cells, and the composition of our blood and fat, according to the study.
Findings were published May 12 in the journal Nature Communications.
It's been known that there are seasonal variations in a number of conditions, including heart disease, autoimmune disorders such as type 1 diabetes, multiple sclerosis and mental illness, as well as in vitamin D metabolism. However, the researchers said this is the first study to show that seasonal changes may affect immune system function.
"In some ways, it's obvious -- it helps explain why so many diseases, from heart disease to mental illness, are much worse in the winter months -- but no one had appreciated the extent to which this actually occurred," said John Todd, professor and director of the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory at the University of Cambridge.
"The implications for how we treat disease like type 1 diabetes, and even how we plan our research studies, could be profound," he said in a university news release.
One gene that was more active in the summer and less active in the winter has been shown to suppress inflammation in mice. If the same is true in people, those in the Northern Hemisphere would have higher levels of inflammation in the winter.
Inflammation is a risk factor for a number of diseases, which means that those at high risk might be more likely to have more health problems during the winter. Drugs that target inflammation may offer a way of treating these diseases more effectively in the colder months, the researchers suggested.
They also found that certain genes associated with people's responses to vaccines were more active in winter. This means that some vaccination programs might be more effective during that season.
"Given that our immune systems appear to put us at greater risk of disease related to excessive inflammation in colder, darker months, and given the benefits we already understand from vitamin D, it is perhaps understandable that people want to head off for some 'winter sun' to improve their health and well-being," Todd said.
Exposure to sun triggers vitamin D production in the body.
Source: HealthDay Copyright © 2015 HealthDay (13/05/15)
People with celiac disease may be at higher risk of neuropathy, according to a new study published in JAMA Neurology.
Celiac disease can affect everyone differently, meaning it can be tricky to diagnose. However, digestive symptoms - such as diarrhea, vomiting, abdominal bloating and pain and weight loss - are most common in children, while adults with the condition are more likely to experience fatigue, bone or joint pain, arthritis or other non-digestive symptoms.
It is estimated that around 1% of the US population - the equivalent to 1 in 133 Americans - have celiac disease, though it is thought around 83% of these individuals are undiagnosed or misdiagnosed with other illnesses.
The association between celiac disease and neuropathy, or nerve damage, is not new. According to the researchers of this latest study, including Dr. Jonas F. Ludvigsson of the Karolinska Institutet in Stockholm, Sweden, it was first identified almost 50 years ago.
Untreated celiac disease has also been linked to increased risk of nerve-related conditions, such as multiple sclerosis (MS).
For their study, Dr. Ludvigsson and colleagues set out to determine the absolute and relative risk of neuropathy among a nationwide population-based sample of patients with a confirmed diagnosis of celiac disease.
2.5-fold increased neuropathy risk for patients with celiac disease
The study included 28,232 individuals from Sweden whose celiac disease was confirmed with small-intestine biopsies, alongside 139,473 age- and sex-matched controls.
The researchers identified 198 (0.7%) participants with celiac disease who were later diagnosed with neuropathy, while neuropathy was later diagnosed in 359 (0.3%) of control participants.
The team calculated that overall, participants with celiac disease were around 2.5 times more likely to receive a later diagnosis of neuropathy than those without celiac disease.
The absolute risk of developing neuropathy was estimated to be 64 per 100,000 person-years among participants with celiac disease, while the absolute risk of neuropathy was estimated at 15 per 100,000 person-years among participants free of celiac disease.
Commenting on their findings, the researchers say:
"We found an increased risk of neuropathy in patients with celiac disease that persists after celiac disease diagnosis. Although absolute risks for neuropathy are low, celiac disease is a potentially treatable condition with a young age of onset."
The team adds that the study indicates patients with neuropathy should be screened for celiac disease.
In November 2014, Medical News Today reported on a study suggesting that some non-gluten wheat proteins may trigger celiac disease.
Published in the Journal of Proteome Research, the study revealed that non-gluten proteins including serpins and purinins triggered a greater immune reaction among patients with celiac disease and dermatitis herpetiformis - a rash associated with the disease - than among those without such conditions.
Source: MNT © 2004-2015 MediLexicon International Ltd (13/05/15)
Blood test study findings revealed(12/05/15)
Amarantus BioScience Holdings says it has reported preliminary data from the blood-based version of its MSPrecise® diagnostic, the Company's proprietary multiple sclerosis (MS) diagnostic test.
MSPrecise, a next-generation DNA sequencing (NGS) assay, measures DNA mutations found in rearranged immunoglobulin genes in immune cells (B cells) to identify patients with relapsing-remitting multiple sclerosis (RRMS) at first clinical presentation.
Results from the most recent MSPrecise validation study using cerebrospinal fluid (CSF) samples for MS, reported in January 2015, demonstrated an 86 per cent sensitivity and 71 per cent specificity in correctly identifying early-stage RRMS in subjects being evaluated for a demyelinating disease undergoing the current diagnostic standard of care (clinical evaluation, magnetic resonance imaging and oligoclonal banding tests), as adjudicated by an expert panel of physicians. When combined with oligoclonal banding tests (OCB), sensitivity improved to 96 per cent and specificity improved to 83 per cent.
In the study, preliminary results indicate the MSPrecise blood assay exhibited an 81 per cent sensitivity and 89 per cent specificity for identifying early-stage RRMS in subjects being evaluated for a demyelinating disease undergoing the current diagnostic standard of care. These results have not yet been combined with OCB and will require replication prior to moving into a CLIA validation study.
"These early findings are encouraging, and provide a pathway to further define and refine the MSPrecise blood assay," said Colin Bier, Chief Development Officer of Amarantus Diagnostics.
"Of particular importance, in this initial blood study, is the promising and positive analytical performance. There is such a high rate of misdiagnosis of MS, especially upon first clinical presentation of this chronic and extremely debilitating disease, that a blood test would be of great benefit to patients and physicians. We are preparing MSPrecise CSF for a CLIA-enabling validation study and, in parallel, will actively continue research and development of the MSPrecise blood assay."
Source: Nasdaq GlobalNewswire © 2015 GlobeNewswire, Inc (12/05/15)
A new study has put forward the suggestion of a relationship between mood disorders, suicidal thoughts, substance abuse and problem drinking in people with MS.
Researchers Susan Quesnel and Anthony Feinstein of the Department of Psychiatry, University of Toronto and Sunnybrook and Women’s College Health Science Centre in Ontario, Canada, sought to find out more about problem drinking, depression and suicide in people with MS.
The pair studied drinking patterns in 140 multiple sclerosis patients. The researchers sought to determine whether study participants had a lifetime history of psychiatric diagnoses using a standard assessment called the Structured Clinical Interview for DSM-IV disorders (SCID-IV). The DSM-IV refers to the Diagnostic and Statistical Manual of Mental Disorders used by clinicians and psychiatrists to diagnose psychiatric illness.
The research revealed that one in every six MS patients drinks to excess over the course of their lifetime. Those people with a history of problem drinking also had a higher lifetime prevalence of anxiety, but not mood disorders such as depression. In addition, people with a drinking problem also were more likely to have had suicidal thoughts over the course of their lifespan, as well as other substance abuse problems and a family history of mental illness. The researchers found that all of these associations were statistically significant.
In their report, the researchers said: “Clinicians should be aware of the possibility of problem drinking in MS patients, and how this may complicate the course of their disease. Clues to problem drinking in MS patients are the presence of a positive family history of mental illness and prominent anxiety.”
The researchers said comprehensive care of MS should ideally include monitoring for other commonly associated problems, such as depression, suicidal thoughts, drinking problems and anxiety. Understanding risk factors for the occurrence of these problems in MS can help patients and their families alike.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (12/05/15)
Childhood multiple sclerosis often goes undetected but Lucy Wood's early diagnosis at the age of five has been crucial in reducing her disability over time.
A photograph of 11-year-old Lucy Wood taken last September shows her smiling in her new uniform, ready for her first day at secondary school. In another photo she is wearing the same smile but is hooked up to a hospital drip as she receives her monthly dose of Tysabri, the drug that controls her multiple sclerosis.
Diagnosed with MS at the age of five, Lucy is one of fewer than 10 per cent of patients who suffer their first symptoms in childhood: most of the 100,000 people with the disease in the UK develop it in their 20s and 30s. She was lucky, however, to receive an early diagnosis. New research from the University of Manchester has found that childhood MS often goes undetected, sometimes for years.
According to lead author Professor Susan Kirk, the delay is due to “low levels of awareness in the general public and doctors about the existence of childhood MS,” as well as there being only “a small group of paediatric neurologists with the necessary expertise to make the diagnosis.”
While some 125 children under 15 in the UK experience a first MS-like “attack” each year – commonly a problem with vision - only around 20 per cent subsequently develop paediatric MS.
Doctors do not know why an initial attack is followed by further attacks in some children but not in others.
Lucy, from Peterlee in county Durham, was three when she experienced a temporary loss of vision in her left eye. Doctors suspected a rare nervous system disease called ADEM (Acute Disseminated Encephalomyelitis), which can cause similar symptoms to MS and which was successfully treated with steroids. Further problems with Lucy’s vision, balance, coordination and speech followed, but her parents were still told MS was unlikely. This was even though Lucy’s father, Stuart, 46, had been diagnosed with MS aged 27 – and having a parent with MS increases the risk from 1 in 600 to 1 in 50.
“We were told MS was incredibly unusual at Lucy’s age, but to me it was like watching Stuart develop the disease all over again. We became convinced our daughter had it,” says Sharon, 45, Lucy’s mother. An MRI scan in August 2008 confirmed Lucy’s parents’ worst fears.
“We expected it but it still felt like a bombshell,” says Sharon. “Stuart blamed himself, believing he must have passed it on. In the end, Lucy’s positive attitude helped him accept it.” The couple’s other daughter, Katie, 17, shows no signs of MS.
Lucy experiences fatigue and sometimes needs to use a wheelchair. But Tysabri, prescribed four years ago to help dampen the immune system’s attack on myelin, has been “life changing”, says her mother.
Dr Cheryl Hemingway, a consultant paediatric neurologist at Great Ormond Street Hospital, runs one of the largest clinics in the country for children with MS and other rare myelin-attacking disorders. Early diagnosis is crucial, she says, for reducing the accumulation of disability over time and enabling children to “get on with their lives.”
Source: The Daily Telegraph © Copyright of Telegraph Media Group Limited 2015 (11/05/15)
Researchers in Denmark say children who have gone through a divorce could be at a slightly increased risk of developing multiple sclerosis.
The study, Stressful Life-Events In Childhood And The Risk Of Multiple Sclerosis: A Danish nationwide Cohort Study, looked at the cases of 2.9m Danes born between 1968 and 2011. A stressful life event (SFLE) was classed as divorce, parental death or the death of a sibling before the age of 18. MS cases in the cohort were identified in the Danish Multiple Sclerosis Registry. Associations of SFLE with MS risk were evaluated by incidence rate ratios (RR) of MS obtained in log-linear Poisson regression models.
Researchers found people exposed to any SFLE in childhood were at 11 per cent elevated risk of MS, compared to the “non-exposed”. Stratification by subtype of SFLE showed parental death and death of a sibling were not associated with MS risk. However, those exposed to divorce were at 13 per cent increased risk of developing MS compared to the “non-exposed”.
Source: University Of Southern Denmark (11/05/15)
Tysabri review launched in Europe(11/05/15)
In light of growing evidence, the European Medicines Agency (EMA) has been asked to launch a review of the multiple sclerosis drug Tysabri to assess whether advice on managing known risks for progressive multifocal leukoencephalopathy (PML) should be revised.
PML is a rare brain infection caused by the JC virus (JCV), which has symptoms that may resemble those of an MS attack and may be fatal or result in severe disability. In addition to the presence of anti-JCV antibodies, other risk factors for PML are treatment duration, especially beyond two years, and immunosuppressant use before receiving Tysabri. Patients with all of the above risk factors have a significantly higher risk for PML.
Tysabri was approved in the European Union in June 2006 as a single disease-modifying therapy in highly active relapsing remitting MS (RRMS). It's indicated for patients with high disease activity despite treatment with a β-interferon or glatiramer acetate and in those with rapidly evolving severe RRMS. Tysabri was first approved by the US Food and Drug Administration (FDA) in November 2004.
The review will involve evaluating the data on the risk for PML, with the aim of better defining the risk and identifying further measures to minimize it and will be carried out by the Pharmacovigilance Risk Assessment Committee (PRAC), which will make a set of recommendations. The PRAC recommendations will then be forwarded to the Committee for Medicinal Products for Human Use.
The final stage of the review procedure is the adoption by the European Commission of a legally binding decision applicable to all EU member states.
The EMA has recently been made aware of new information in three key related issues, a statement from the agency notes:
Risk estimates: Tysabri treatment decisions are based on an algorithm in which the estimated PML incidences are calculated in a static way by pooling data from all sources (clinical studies, registries, spontaneous reports). However, interim data from the STRATIFY 2 study for patients with positive anti-JCV antibody status with and without a history of immunosuppressive treatment suggested a higher risk for PML than currently described in the algorithm.
Diagnosis of PML before the development of clinical symptoms: New data seem to suggest that asymptomatic PML cases have a higher survival rate (95.6 per cent) than do symptomatic cases (77.1 per cent). Current recommendations are to perform MRI within 3 months before initiating treatment and then annually. Recent literature suggests that more frequent MRI testing may detect a greater proportion of asymptomatic cases.
Anti-JCV antibodies: It was thought that a negative serologic anti-JCV antibody test suggested a very low probability of PML (about 0.01 per cent), but evidence from the AFFIRM and STRATIFY 1 studies showed nearly 13 per cent of negative patients could become positive during follow-up.
Currently, it's recommended that these patients be retested every six months for antibodies, but a more sensitive second-generation enzyme-linked immunosorbent assay was recently developed. Whether this affects current recommendations for antibody testing needs to be assessed.
Tysabri is a monoclonal antibody, administered through intravenous injection, that is designed to recognize and attach to a protein on the surface of leucocytes. By blocking this protein, the drug prevents leukocytes from going from the blood to the brain, thereby reducing inflammation and nerve damage caused by MS.
Source: Medscape Multispeciality Copyright © 1994-2015 by WebMD LLC (11/05/15)
Researcher takes sharper look at MS(07/05/15)
A young researcher at Massachusetts General Hospital is exploring ways to diagnose and track multiple sclerosis more accurately with stronger and faster imaging technologies.
Using ultra high-resolution magnetic resonance imaging (MRI) at Massachusetts General Hospital, a physician-scientist in the MGH Multiple Sclerosis Clinic is pioneering revolutionary new ways to see the disease in the brains of human patients. Ultimately, this improved imaging may permit doctors to more accurately track the disease in patients with multiple sclerosis (MS) and find ways to provide faster, better treatment and earlier diagnosis.
“MRI has really revolutionised the way we assess MS,” says Eric C. Klawiter, MD, assistant neurologist in Mass General’s Department of Neurology, who is leading efforts to use new MRI technologies to help MS patients.
Dr. Klawiter is also working with a super-fast MRI scanner unique to Mass General to study connections in the living brain. Developed as part of the National Institutes of Health Human Connectome Project, it’s a remarkable tool for MS research. Currently, a pilot study comparing brain connectivity data from healthy subjects and people with MS is underway, Dr. Klawiter says. It could yield clues for treating cognitive problems, which affect roughly half of people with MS.
Additionally, Dr. Klawiter hopes to use the scanner to develop reliable markers for MS, such as one that helps identify when myelin is being stripped away. A similar marker for axon damage, which may correlate with disability, might be even more useful. Finding these markers can greatly accelerate drug development. In addition, these imaging breakthroughs could lead to earlier diagnosis, which could allow doctors to take preventive steps that will help patients before the disease begins to take its toll.
Source: Massachusetts General Hospital © 2015 Massachusetts General Hospital (07/05/15)
A drug developed from the toxin of a sea anemone to treat conditions such as multiple sclerosis have shown promise in a phase 1 clinical trial, it has been reported.
The drug, dalazatide, is being developed by Kineta Inc, and works differently from drugs currently used to treat immune disorders. They suppress the entire immune system, which puts patients at risk for infections, while dalazatide blocks only the white blood cells that trigger many autoimmune diseases.
"The results of this trial indicate an important advance in developing next-generation treatments for autoimmune disease that specifically regulate the immune response without broad immune suppression," Dr. Shawn Iadonato, Kineta’s chief scientific officer, told the Wall Street Journal.
Phase 1 trials are designed to test a drug's safety and tolerability using various dosages. Tested on patients with psoriasis, the group were given either 30 mg or 60 milligrams of dalazatide or a placebo by injections twice a week for four weeks.
Even though phase 1 trials are designed to test a drug's safety and tolerability, patients who received dalazatide, especially those getting the higher dosage, showed improvements in their psoriasis that continued during the month after the drug was stopped. In contrast, those patients taking a placebo experienced no changes.
Kineta hopes to begin recruiting patients next year for a phase 2 trial which will specifically test the drug's effectiveness.
The development of dalazatide is part of an ongoing effort to create medicines, including painkillers, from nature. Researchers have found, for example, that certain kinds of spider venom block the pathway that sends signals of pain from the nerves to the brain in a way that is non-addictive.
Source: Newsmax Health © 2015 NewsmaxHealth (06/05/14)
A study, Human Placenta-Derived Cells (PDA-001) For The Treatment Of Adults With Multiple Sclerosis: A Randomised, Placebo-Controlled, Multiple-Dose Study, published in the journal Multiple Sclerosis and Related Disorders and led by researchers at Mount Sinai in New York and Celgene Cellular Therapeutics, has revealed an infusion based on cells derived from the placenta proved to be safe for patients with multiple sclerosis and a promising new treatment for the condition.
It has been previously shown that therapeutic cell-based infusions have an immunomodulatory and repair action in MS. PDA-001 in particular is a preparation of cultured mesenchymal-like cells derived from healthy human placental tissue and designed for the treatment of MS as these cells have immunomodulatory, anti-inflammatory, pro-regenerative and neuroprotective properties. As these placenta cells are expanded in cell culture, one healthy donor is capable of supplying enough cells for several patients.
In the study, researchers tested the safety and possible exacerbation of the disease with this new MS treatment approach based on PDA-001. A phase 1b, randomised, multi-centre, double-blind, placebo-controlled study was conducted with 16 MS patients (ten with relapsing-remitting MS and six with secondary progressive MS), aged between 18 and 65 years. Six patients received a high dose of PDA-001 (600×106 cells), other six were given a lower dose (150×106 cells), and the remaining four patients received a placebo. Patients were monitored monthly for brain lesions.
Researchers found none of the patients had worsening of MS-related brain lesions one year after treatment with both PDA-001 doses, and the majority of the patients had stable or had improved levels of disability.
“We’re hoping to learn more about how placental stromal cells contribute to myelin repair,” said the study’s lead author and Professor of Neurology at Mount Sinai, Dr Fred Lublin in a news release.
“We suspect they either convert to a myelin making cell, or they enhance the environment of the area where the damage is to allow for natural repair. Our long-term goal is to develop strategies to facilitate repair of the damaged nervous system.”
The research team concluded that PDA-001 treatment was overall safe and well tolerated by patients, and that preliminary evidence suggests that PDA-001 could be able to repair damaged nerve tissues in MS patients.
“This is the first time placenta-derived cells have been tested as a possible therapy for multiple sclerosis,” said Dr Lublin.
“The next step will be to study larger numbers of MS patients to assess efficacy of the cells, but we could be looking at a new frontier in treatment for the disease.”
Source: Multiple Sclerosis News Today © BioNews Services 2015 (06/05/15)
Guanabenz studies underway(05/05/15)
The Myelin Repair Foundation (MRF), in partnership with the National Institutes of Health (NIH) has announced patients are now being enrolled in a clinical trial to study guanabenz, an FDA-approved drug to treat high blood pressure that was identified by MRF-funded researchers as a potential therapy to reduce loss of myelin in multiple sclerosis patients.
If successful, guanabenz (formerly called MRF-008) could be the first MS treatment to focus on protecting myelin from damage, which is the hallmark of MS, rather than on suppressing the immune system - as all currently available MS treatments do.
The trial, a collaboration between the MRF and the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NIH) Clinical Centre, is being led by NIH Investigators Dr. Irene Cortese, M.D., and Dr. Daniel Reich, M.D., Ph.D.
Myelin is the membrane that surrounds and protects nerve fibres (axons) in the central nervous system.
In MS patients, the immune system damages myelin and the cells that produce and maintain it (oligodendrocytes). As the disease progresses, severe myelin degeneration is accompanied by axonal loss and neurodegeneration, all of which can profoundly disrupt signalling in the central nervous system and so leading to the array of symptoms that characterises MS.
Because loss of myelin correlates with neurodegeneration, new therapies that are designed to protect myelin or promote remyelination would be categorized as neuroprotective.
In a Nature Communications paper published in March, MRF-funded researchers reported that guanabenz prevents myelin loss and alleviates clinical symptoms of MS in animal models by prolonging an innate mechanism that is activated in response to stressors such as inflammation.
When this protective response is disrupted or overloaded - by the chronic inflammation seen in MS, for example - oligodendrocyte cell death and demyelination are significantly enhanced. Treatment with guanabenz strengthens this stress-response mechanism and helps protect oligodendrocytes from cell death. These findings point to promising avenues for the development of new treatments for MS.
"Guanabenz appears to enhance the cell's own protective machinery to diminish the loss of myelin," said senior study author Brian Popko, Ph.D., Jack Miller Professor of Neurological Disorders at the University of Chicago and a member of the Myelin Repair Foundation's Research Consortium.
"While there have been many efforts to stimulate remyelination, this now represents a unique protective approach. You don't have to repair the myelin if you don't lose it in the first place."
The MRF has supported Dr. Popko's research on the effects of inflammation on oligodendrocyte health and myelin production for more than ten years. In addition to Dr. Popko's team at the University of Chicago, MRF-funded researchers at Northwestern University in Chicago, Case-Western Reserve University in Cleveland, and scientists at the MRF's Translational Medicine Center in Sunnyvale, CA, made key contributions to the guanabenz publication.
The MRF's clinical advisory board reviewed the preclinical data and encouraged the MRF to advance guanabenz into clinical testing. The drug's protective efficacy and ability to alleviate myelin loss, coupled with its existing FDA approval and good safety profile, makes the clinical implications promising for MS patients, the advisory board concluded. However, before clinical studies could be initiated, the MRF had to identify a contract drug manufacturer to make clinical-grade guanabenz.
Because guanabenz has been off the market for many years, it is no longer manufactured anywhere in the world.
"We are very pleased guanabenz is now moving into studies in MS patients," said Tassie Collins, Ph.D., Vice President of Translational Medicine at the Myelin Repair Foundation.
"This is a promising approach, but it might not have been able to move forward without MRF's participation."
Because it is a generic drug, guanabenz would be an unlikely investment choice for pharmaceutical companies. And because it had to be custom-manufactured for the trial, most academic organizations would have been unable to resource it.
Source: Drug Research Drug Discovery & Development © PBR 2015 (05/05/15)
After the Phase 2b clinical trial achieved full enrolment with 190 secondary progress multiple sclerosis (SPMS) patients, Texas-based Opexa Therapeutics is now awaiting results for the company’s lead candidate, Tcelna, which are expected in the second half of 2016.
The therapy, which was spun off from a technology developed at Baylor College of Medicine (BCM) Technologies that was licensed and developed by Opexa, has shown efficacy in both SPMS and relapsing-remitting multiple sclerosis (RRMS) patients in earlier clinical trials.
“We have spent a good decade in clinical trials treating early- and late-stage multiple sclerosis,” said Neil Warma, President and CEO of Opexa Therapeutics, in an exclusive interview with Multiple Sclerosis News Today.
“In true fashion, we are trying to restore function of the immune system via personalized therapies that fight the root cause of disease itself.”
The focus of Tcelna is the interaction between T-cells and the rest of the body.
“It is similar in concept to a T-cell vaccine, but these ‘vaccines’ are personalized for patients with multiple sclerosis,” explained Warma.
“In patients with multiple sclerosis, there is a small population of myelin reactive T-cells (MRTCs) that cross into the central nervous system and attack nerve fibres. We isolate and identify those pathogenic T-cells, attenuate them, and reintroduce them back into the individual.”
First, a sample of blood is taken from a patient and sent to Opexa’s Good Manufacturing Practices (GMP) facility in Houston. Scientists then identify the specific myelin peptide antigens that the patient’s MRTCs recognize.
Out of 109 peptides screened by Opexa, typically three or four peptides are dominant, and are introduced to a population of expanding T-cells. After a few more manufacturing steps to attenuate the reactive T-cells, these are then shipped to the patient’s physician’s office, who receives a subcutaneous injection of the “T-cell vaccine.”
“The injection primes the body to selectively recognize and attack the MRTCs,” said Warma.
“It’s telling the immune system that these attenuated cells should be treated as foreign attackers.”
Although the injection delivers a bolus of MRTCs, the cells are attenuated, meaning they pose no risk of further destroying myelin. Instead, the cells die off and remain in situ long enough for the patient’s immune system to recognize the cells as damaging and harmful. With a heightened immune system, the patient’s own healthy T-regulatory cells search for MRTCs to remove them from the body in a sort of “anti-T-cell T-cell response.”
Traditional therapies wipe out the entire immune system and target all T-cells and other immune cells for destruction. Tcelna targets a select population of MRTCs, giving the treatment a better side effect profile and greater patient tolerability.
“Pharma looks at ‘personalised’ differently,” said Warma.
“They have a drug candidate that is effective in 10-20 per cent of patients, and they segment the market to serve those patients. At Opexa, we look at all multiple sclerosis patients and find a personalized therapy for every individual.”
Personalisation of treatment continues past the first dose. The optimal dosing schedule was found to be five subcutaneous injections each year, given in the first six months. An injection is given at one, two, three, four, and six months. In the next year, the injection pattern is identical, but patients receive a different formulation of T-cells.
“Each of our preparations is tailored specifically to match each individual’s profile. Each patient receives a specialized therapy,” Warma told Multiple Sclerosis News Today.
“Myelin peptide antigens change over time and are different for every individual. In year two, three, and beyond, we conduct the antigen screening process because we know these myelin peptides shift over time. We deliver a specific T-cell vaccine to each individual, relevant at that time.”
Source: Multiple Sclerosis News Today © BioNews Services 2015 (05/05/15)
Cytokines may play major role in MS(29/04/15)
Researchers say they have discovered the role of a major cytokine in multiple sclerosis that could be a target for new therapy against the disease.
MS is caused by immune cells that activate a cascade of chemicals in the brain, attacking and degrading the insulation that keeps neuronal signals moving. These chemicals, called cytokines, drive the inflammation in the brain, attracting more immune cells, and so causing the condition.
Researchers have long debated which cytokines drive the condition and which are merely accessory. Now a study published in the Journal of Immunology confirms the cytokine GM-CSF (Granulocyte macrophage colony-stimulating factor) likely plays an important role in human disease and offers a new explanation for why the MS treatment interferon-Beta is often so effective.
"After our animal studies showed GM-CSF was important in the development of an MS-like disease, we were excited to see these results confirmed using samples from MS patients in the current study," says Abdolmohamad Rostami, M.D., Ph.D., Chair of the Department of Neurology at Thomas Jefferson University and director of its neuroimmunology laboratory.
A few years ago, MS researchers were focused on a new type of immune cell called the Th-17 cell, which appeared to be a key player in driving the neuronal damage in MS. Because Th-17 cells produce the cytokine IL-17, researchers likewise thought this chemical was essential to the condition. IL-17, however, turned out to be something of a red herring.
In a paper published in Nature Immunology in 2011, Dr. Rostami and colleagues showed the Th-17 cells also produced another cytokine called GM-CSF, which created a chain reaction with another cell type ultimately increasing the GM-CSF levels in the brain of mouse models significantly. In addition, the researchers showed that in experimental models of MS, mice that were unable to produce GM-CSF never developed the condition, whereas mice lacking IL-17 did develop the disease, though generally developed a milder form.
In the new study, to test whether the same observation was true in humans, Dr. Rostami and colleagues tested blood samples of patients with MS who had not yet received therapy, and those currently being treated with interferon-Beta, a commonly used therapy. On average, untreated patients had two to three times as many immune cells producing GM-CSF as did patients being treated with interferon-Beta, or normal subjects. In addition, the researchers looked at brain samples of deceased patients with MS and found increased numbers of GM-CSF-producing cells in comparison to normal brain samples.
"The study demonstrates a new mechanism of action for interferon-Beta therapies," says Dr. Rostami.
In addition, a recent Phase 1 clinical trial of an antibody that blocks GM-CSF showed early signs of effect. Phase 1 trials are typically only designed to determine if a new drug is safe, and can't answer whether a new drug works. However, these results together with the work from the Rostami lab suggest that GM-CSF is a target worth pursuing for the treatment of MS.
"We hope that this research showing GM-CSF is an important target will lead us toward therapies that more effectively block the damaging immune reaction in the central nervous system of MS patients," says Dr. Rostami.
Source: EurekaAlert! Copyright © 2015 by the American Association for the Advancement of Science (AAAS) (29/04/15)
A Buckinghamshire charity is trying to show us how the people they treat are not all the same, despite stereotypes.
This National MS Awareness week sees the launch of a campaign by the Chilterns MS Centre in Wendover called #30talkingheads which challenges the preconceptions surrounding multiple sclerosis (MS).
MS affects 1 in 600 people in the UK and 100 people are diagnosed with it every week but the Centre feels there is still a lack of awareness and understanding about the disease.
The Chilterns MS Centre is a local independent charity that provides therapy and treatment for 300 people each week. Their montage of photos of 30 Centre members shows the diversity of people with MS.
The concept of the campaign is to show that Multiple Sclerosis affects more women than men and that some are young while some have a few more miles on the clock! It also portrays that, despite people’s misconceptions, most people diagnosed with MS do not need to use a wheelchair on a regular basis.
Each person with MS is very different both in terms of themselves as individuals but also in terms of the symptoms they have and the course of the disease.
Some of those symptoms could be subtle and often hidden like fatigue and problems with vision whereas some are noticeable like issues with mobility and balance.
As part of the campaign the members were asked what the disease and what the Chilterns MS Centre meant to them.
Just like the uniqueness of the people involved and their MS, they all have a different take on how it has affected them but a resounding theme was that the Chilterns MS Centre provides excellent care and support.
Mark Webb said: “MS is companion for life I never asked for or expected, wrenching so much away. But offering new opportunities and real friends through the Centre”
Maria De Courcy said: “MS is life changing in many ways so I learn to live with MS as a new way of living. It can be tough sometimes but life is a challenge and challenges are there to be conquered. I guess it’s about finding the right support like the Centre. If you have that you can get through most things that life throws at you!”
Sarah Jones said: “My life experience changed so much since my diagnosis of MS. I have learnt so much about myself, experienced such kindness and met some wonderful people at the Chilterns MS Centre”
Source: Mix 96 Copyright Mix 96 2015 (29/04/15)
Fingolimod efficiently reduces multiple sclerosis (MS) relapse by inhibiting lymphocyte egress from lymph nodes through down-modulation of sphingosine 1-phosphate (S1P) receptors. We aimed to clarify the alterations in peripheral blood T cell subsets associated with MS relapse on fingolimod.
Blood samples successively collected from 23 relapsing-remitting MS patients before and during fingolimod therapy (0.5 mg/day) for 12 months and 18 healthy controls (HCs) were analysed for T cell subsets by flow cytometry. In MS patients, the percentages of central memory T (CCR7+CD45RO+) cells (TCM) and naïve T (CCR7+CD45RO-) cells decreased significantly, while those of effector memory T (CCR7-CD45RA-) and suppressor precursor T (CD28-) cells increased in both CD4+T and CD8+T cells from 2 weeks to 12 months during fingolimod therapy. The percentages of regulatory T (CD4+CD25highCD127low) cells in CD4+T cells and CCR7-CD45RA+T cells in CD8+T cells also increased significantly. Eight relapsed patients demonstrated greater percentages of CD4+TCM than 15 non-relapsed patients at 3 and 6 months (p=0.0051 and p=0.0088, respectively). The IL17-, IL9-, and IL4-producing CD4+T cell percentages were significantly higher at pre-treatment in MS patients compared with HCs (p<0.01 for all), while the IL17-producing CD4+T cell percentages tended to show a transient increase at 2 weeks of fingolimod therapy (pcorr=0.0834).
The CD4+TCM percentages at 2 weeks to 12 months during fingolimod therapy are related to relapse.
Source: PLOS One (29/04/15)
Scientists from the Gladstone Institutes have discovered a way to prevent the development of multiple sclerosis in mice. Using a drug that blocks the production of a certain type of immune cell linked to inflammation and autoimmunity, the researchers successfully protected against the onset of MS in an animal model of the disease. The scientists say the next step is to test this strategy using other autoimmune disorders.
"We are very excited about these findings," says Eric Verdin, MD, a senior investigator at Gladstone and co-senior author on the study.
"In light of the significant effect the treatment had on inflammation, the implications of these results will likely extend beyond multiple sclerosis to other types of autoimmune disorders. We are particularly interested in testing this in type I diabetes given the similar pathways involved, and we are already seeing very promising results in preliminary experiments."
In the immune system, two kinds of T cells strike a delicate balance - T helper cells (Th17) activate the immune system, protecting against infections and cancers, while regulatory T cells (Tregs) suppress the system, keeping it in check. A disparity between these cell types, where there are too many Th17 and not enough Tregs, can lead to a hyperactive immune system, resulting in inflammation, tissue damage, and autoimmune disease.
In the current study, published in the Journal of Experimental Medicine, the researchers discovered that an important regulatory protein, sirtuin 1 (SIRT1), is involved in the production of Th17 cells. By blocking this protein, the scientists can protect against the onset of autoimmunity. SIRT1 also has a negative impact on Treg maturation and maintenance, so inhibiting its expression simultaneously enhances the production of Tregs and suppresses the creation of Th17.
To test this effect on disease, the researchers used a mouse model of MS and treated the animals with a drug that inhibits SIRT1. Typically, MS-model mice experience severe motor problems, eventually leading to paralysis, but when they were given the drug the mice behaved perfectly normally. Moreover, the treated animals showed no signs of inflammation or cell damage in their spines, classic markers for MS.
In contrast with the current research, SIRT1 is typically thought of as having anti-inflammatory properties, and compounds that increase SIRT1, like resveratrol, have been proposed as a way to delay aging. However, first author Hyungwook Lim, PhD, a postdoctoral fellow at Gladstone, says the new research suggests that the protein's effects are more complicated.
"The conventional theory has been that you should activate SIRT1 to improve health and longevity, but we show that this can have negative consequences," says Dr. Lim.
"Instead, we think the role of SIRT1 very much depends on the type of tissue being targeted. For instance, in immune cells, instead of being anti-inflammatory SIRT1 appears to have a pro-inflammatory role, which makes it a prime target to treat autoimmune disorders."
Other Gladstone investigators on the study include Jae Kyu Ryu, Mingjian Fei, Intelly Lee, Kotaro Shirakawa, Herbert Kasler, Hye-Sook Kwon, Katerina Akassoglou, and Melanie Ott, who was a co-senior author on the paper. Scientists from the University of California San Francisco, Scripps Research Institute, Buck Institute for Research on Aging, National Institute of Infectious Diseases Japan, German Cancer Research Center, New York University School of Medicine, and Howard Hughes Medical Institute also took part in the research. Funding was provided by the Kurtzig and Mulholland families, the National Center for Research Resources, and the National Center for Biotechnology Information.
Source: EurekaAlert Copyright © 2015 by the American Association for the Advancement of Science (AAAS) (27/04/15)
There has been an “alarming rise” in the cost of multiple sclerosis treatments over the past dozen years and the cost of these drugs increased at rates well beyond the overall growth in prescription drug prices, according to a new study.
Reporting on the Pharmalot medical blog, Ed Silverman says the study found costs for three older medicines, which were launched between 1993 and 1996, rose by statistically significant amounts after a new type of treatment became available in 2002.
And a similar pattern of rising costs continued as still newer medications were approved by regulators between 2010 and 2013, according to the study, which appears in the Neurology medical journal.
“Instead of dropping back or stabilising as newer drugs became available, the prices for older medicines continued to rise, notably for the older medications,” says Dennis Bourdette, who chairs the neurology department at Oregon Health & Science University and is a co-author of the study.
“You would think more new drugs would lower the rate of the increases, but that didn’t happen.”
The study also compared prices paid by Medicaid, the U.S. Department of Veterans Affairs and government purchasers in Canada, the U.K. and Australia. Although Medicaid receives discounts, the costs for the multiple sclerosis treatments were often more than 70 per cent lower in the other countries than what was paid by Medicaid. The VA, meanwhile, paid 36 per cent less, on average, than Medicaid.
The findings are the latest attempt to track rising costs for prescription medicines. Until now, the discussion has largely focused on treatments for hepatitis C, and cancer, as well some generic drugs. Bourdette says this is the first effort of its kind by neurologists to highlight the upward trend in multiple sclerosis drug costs.
The study examined pricing data for nine multiple sclerosis treatments – including older injectable medicines and newer oral drugs – between 1993 and 2013. The researchers also compared prices for the older drugs with another group of injectable medicines used to treat rheumatoid arthritis that were available during this time and found price hikes were much higher for the MS drugs.
More specifically, the study found three so-called first-generation MS treatments, which originally cost between $8,000 and $11,000 annually, now cost about $60,000. This worked out to an average increase of 21 per cent to 36 per cent annually for these three injectable drugs, which include Betaseron, which is sold by Bayer, Avonex, marketed by Biogen, and Copaxone, a big seller for Teva Pharmaceutical.
The cost increases for these drugs corresponded with the 2002 approval of Rebif, which is sold by Merck Serono, according to the study. And the trend continued with still newer oral drugs that were approved by the FDA between 2010 and 2013. These newer meds included Gilenya, which is marketed by Novartis, Aubagio, sold by Sanofi’s Genzyme unit, and Tecfidera, another Biogen medicine.
A Teva spokesman said pricing is competitive to other brand-name drugs and reflects investment to research, develop and sell a safe and effective product. A Bayer spokesman told Silverman that Betaseron pricing reflects its “value” and is “comparably” priced. A Biogen spokesman, meanwhile, said the drug maker provides discounts and revenues are used to fund research for new drugs.
Meanwhile, prices for the newer oral medications rose eight per cent to 17 per cent annually since their approvals over the past few years compared with overall prescription drug inflation of three-five per cent, according to the study.
“If the prices for the older drugs hadn’t been raised so dramatically, the newer drugs would have had a more difficult time pricing them as high as they did,” says Bourdette. “These companies didn’t have to price them at a lower level, because the prices for the older drugs were steadily being increased. What they’re doing is feeding off each other in terms of how the prices are set.”
Source: The Wall Street Journal Copyright ©2015 Dow Jones & Company, Inc (27/04/15)
MS drug breakthrough by French firm(27/04/15)
French biotechnology company MedDay has announced encouraging results for a multiple sclerosis drug trial, saying it decreased its progress and in some cases led to a “significant improvement” for patients.
“This is the first time a drug has been able to decrease the rate of disease progression in addition to improving a significant proportion of patients with progressive MS," said MedDay CEO Frederic Sedel in a statement.
The experimental drug MD1003 has undergone Phase III clinical trial, the last stage before filing for authorisation to market the drug in the treatment of primary and secondary progressive multiple sclerosis.
The results of the study, presented to the annual meeting of the American Academy of Neurology, were encouraging, said Professor Ayman Tourbah, the study's principal investigator.
“The rapid rate of recruitment into this multi-centre study illustrates the serious need for a well-tolerated drug by patients with primary and secondary progressive multiple sclerosis,” he added in the company's statement.
“The significant proportion of patients showing improvement at twelve months, coupled with the decrease in risk of disease progression demonstrated here, makes MD1003 a potentially important new therapy for patients and in the field of MS.”
The application process to license the drug will begin when all the test results are in, expected by the end of the year.
Source: Malaymail Online Copyright © 2015 Malay Mail Online (27/04/15)
Genzyme has announced new magnetic resonance imaging (MRI) data from the Lemtrada clinical development program.
In relapsing remitting multiple sclerosis (RRMS) patients treated with Lemtrada in the Phase III pivotal studies, MRI effects observed in the two-year trials were maintained through two additional years in the extension study (years three and four). After the initial two courses of treatment in the pivotal studies, which were given at month zero and at month 12, approximately 70 percent of Lemtrada patients did not receive additional Lemtrada treatment during the following three years, through month 48.
The Phase III trials of Lemtrada were randomized, two-year pivotal studies comparing treatment with Lemtrada to high-dose subcutaneous interferon beta-1a (Rebif) in patients with RRMS who had active disease and were either new to treatment (CARE-MS I) or who had an inadequate response to another therapy (CARE-MS II).
Through year four, the adverse event profile of Lemtrada was consistent with that observed during the pivotal studies. The new data includes:
The rate of brain atrophy, as measured by brain parenchymal fraction (BPF), decreased progressively over four years among Lemtrada patients in CARE-MS I. Among CARE-MS II Lemtrada patients, the rate of brain atrophy decreased progressively over three years and remained low in year four. In both studies, the median yearly brain volume loss was less than -0.20% in years three and four, which was lower than what was observed during the two-year pivotal studies.
In CARE-MS I and II, treatment with Lemtrada significantly reduced the risk of developing new lesions compared to interferon beta-1a. In the extension study, most of the Lemtrada-treated patients from CARE-MS I and II were free of new lesions and MRI activity in years three and four (approximately 70%).
Brain atrophy is a measure of the most destructive pathological processes that occur in MS.1 It is seen from the earliest stages of disease and may lead to irreversible neurological and cognitive impairment. Given its association with disability, control or prevention of brain atrophy is an important target for MS treatment. In addition, MRI measures including lesion activity are considered useful tools when evaluating the effect of MS therapies, and lesion activity is among several prognostic factors for unfavorable clinical outcomes.
“It is very promising that most Lemtrada patients experienced slowing of brain atrophy and remained free of new lesions despite receiving their last treatment course three years previously,” said Dr. Alasdair Coles, Professor, Department of Clinical Neurosciences, University of Cambridge. “These new MRI data are consistent with the clinical data from the extension study that provide additional evidence of the sustained efficacy of Lemtrada on both relapses and disability.”
Safety results from the second year of the extension study were previously reported. No new risks were identified. The most common side effects of Lemtrada are rash, headache, pyrexia, nasopharyngitis, nausea, urinary tract infection, fatigue, insomnia, upper respiratory tract infection, herpes viral infection, urticaria, pruritus, thyroid gland disorders, fungal infection, arthralgia, pain in extremity, back pain, diarrhea, sinusitis, oropharyngeal pain, paresthesia, dizziness, abdominal pain, flushing, and vomiting. Other serious side effects associated with Lemtrada include autoimmune thyroid disease, autoimmune cytopenias, infections and pneumonitis. A risk management program incorporating education and monitoring helps support early detection and management of these identified risks.
“The four-year MRI data support the prolonged efficacy of Lemtrada,” said Genzyme President and CEO, David Meeker, M.D. “These results are encouraging, as they provide further evidence of Lemtrada’s potential to change the treatment approach for people living with relapsing forms of MS.”
More than 90 percent of the patients who were treated with Lemtrada in the CARE-MS Phase III trials enrolled in the extension study. These patients were eligible to receive additional treatment with Lemtrada in the extension study if they experienced at least one relapse or at least two new or enlarging brain or spinal cord lesions. MRI scans were taken at CARE-MS baseline, and at 12, 24, 36 and 48 months.
In CARE-MS I, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates; the difference observed in slowing disability progression did not reach statistical significance. In CARE-MS II, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates, and accumulation of disability was significantly slowed in patients given Lemtrada vs. interferon beta-1a.
Source: Market Watch Copyright ©2015 MarketWatch, Inc (24/04/15)
Multiple sclerosis patients who consumed larger amounts of alcohol had lower rates of disability per the Expanded Disability Status Score (EDSS) and Multiple Sclerosis Severity Score (MSSS), a new study indicates.
Consumption of beer also affected EDSS scores positively; however consumption of wine had no association with EDSS score, according to Camilio Diaz-Cruz, MD, of Brigham and Women's Hospital in Boston, who reported the findings at the American Academy of Neurology 2015 Annual Meeting.
Camilio and colleagues measured alcohol/wine consumption in servings per week for 908 patients enrolled in the Comprehensive Longitudinal Investigation of Multiple Sclerosis (CLIMB) study. Drinking habits were also assessed, and influence of alcohol or wine consumption on clinical outcomes was assessed using regression models for relapse rate in the past year, and concurrent EDSS and MSSS outcomes. Associations with and changes in Symbol Digit Modality Tests (SDMT) were also assessed in a subset of patients.
There were 56 nondrinkers in the cohort; 98 of who preferred spirits, 249 preferred beer, 283 preferred red wine, and 222 favoured white wine. Median alcohol intake was 1.1 servings per week.
Those who had higher alcohol intake were significantly associated with lower EDSS and MSSS. Both red and white wine had a non-significant negative association with both EDSS and MSSS, and there was no significant association between alcohol or wine consumption and relapse rate in the past year, change in EDSS or MSSS over one year, current SDMT score, and change in SDMT score in the last year. Notably, beer drinkers tended to have lower EDSS, however the relationship was weaker compared to that of “hard liquor”.
Although further data analyses are required to better understand the potential cause-effect relationship and underlying mechanism, the findings are complimentary to several previous but unconfirmed studies that suggest alcohol may be neuroprotective in the risk of developing multiple sclerosis.
Source: Neurology Advisor Copyright © 2015 Haymarket Media, Inc (24/4/15)
Teva has announced new data on the safety and efficacy of Copaxone (glatiramer acetate injection) 40mg/mL in patients with relapsing forms of multiple sclerosis (MS).
In the 36-month placebo-controlled and open-label extension phases of the Glatiramer Acetate Low-frequency Administration (GALA) study, outcomes of early start (ES) patients who received three-times-a-week Copaxone 40mg/mL for 36 months were compared to delayed start (DS) patients who initiated Copaxone after the 12-month placebo-controlled phase of the trial. The adjusted mean annualized relapse rate was significantly lower for the ES patients over 36 months and early treatment was associated with a sustained reduction in lesion activity and the evolution of active lesions to chronic black holes.
Copaxone is indicated to reduce the frequency of relapses in patients with relapsing-remitting MS, including those who have experienced a first clinical episode and have MRI features consistent with MS.
Source: MPR Copyright © 2015 Haymarket Media, Inc (24/04/15)
Patients with multiple sclerosis (MS) often have sensitivity to heat that worsens their symptoms.
In earlier studies with MS patients a device system that cools body temperature by chilling one palm proved useful in helping them walk faster and longer.
But in a study reported during a poster session April 22 at the 2015 American Academy of Neurology annual meeting in Washington, DC, a California team of researchers found that having the device did not motivate patients to walk more.
Andrew Dorsch, MD, and colleagues at the University of California Los Angeles Health System recruited 24 ambulatory MS patients with heat sensitivity for the study. The subjects were fitted with wireless sensors. They were worn for a week to get a baseline level of physical activity. The patients were then randomly assigned to get either the device or a sham device.
The hope was that the patients with the cooling device would increase their level of exercise. But that did not happen. “Use of a hand-held cooling device was not associated with changes in walking performance,” the team wrote.
But they did find that wireless health technologies are useful in measuring such activities.
Source: MD All Specialities Copyright HCPLive 2006-2015 Intellisphere, LLC (24/04/15)
Freedom from relapse was maintained in multiple sclerosis patients on Tysabri who received the infusion drug less frequently than the recommended 4-week interval, with lower risk of progressive multifocal leukoencephalopathy (PML), preliminary results from an ongoing analysis have indicated.
Among 886 patients treated with "extended" dosing at 10 American MS centers, the mean annualized relapse rate was the same at 0.1 per year as in 1,078 patients receiving Tysabri at the standard 4-week interval, according to Lana Zhovtis-Ryerson, MD, of NYU Langone Medical Center in New York City. MRI lesions counts were also similar.
Although patients testing positive for the JC virus - the pathogen whose reactivation triggers PML, a sometimes fatal brain inflammation - comprised 59 per cent of the extended dosing group, none have so far developed PML, she reported to the American Academy of Neurology's annual meeting.
With a total of 1,023 patient-years of exposure to Tysabri in this JC-positive subgroup, published risk algorithms show an expected incidence of 2.5 cases, Zhovtis-Ryerson and colleagues calculated.
At this point the finding of zero cases with extended dosing is not statistically significant, the researchers cautioned - but if the exposure reaches 1,248 patient-years with still no cases, it will be significant.
Meanwhile, two PML cases have developed in the standard-dosing group, among whom 41 per cent are JC-positive and who have received a mean of 30 Tysabri doses (SD 22).
Brian Weinshenker, MD, of the Mayo Clinic, who was not involved with the study, told MedPage Today the approach deserves more study but urged caution in adopting it clinically.
He noted if just one patient in the extended dosing group developed PML, "it would have completely negated any trend to reduced risk."
PML has been the primary concern with Tysabri almost since it was introduced in 2004. When several cases turned up shortly after its approval, the drug was withdrawn for some months, then relaunched with a restricted distribution program that included clinician and patient education on the risk.
The question of how to reduce PML risk with Tysabri, which exceeds one per cent in patients positive for JC virus and who have two other risk factors (treatment duration and history of immunosuppressant therapy), has occupied MS neurologists since the relaunch. Most studies have shown patients who discontinue the drug or take long "holidays" experience a spike in relapse risk. Switching to another drug has not prevented such spikes because a months-long washout period after Tysabri discontinuation is needed before starting a different agent.
Some clinicians have been experimenting instead with longer dosing intervals, in the belief that the four-week schedule keeps the drug's target - alpha4beta1 integrin, an adhesion molecule involved in immune cell trafficking - so saturated that JC virus immune surveillance is eliminated. Extending the interval may relax the immune suppression just enough to keep latent JC virus under control while still maintaining the anti-relapse effect.
In the current study, Zhovtis-Ryerson and colleagues sought to capture this empirical experience by canvassing centers that have adopted the strategy with some patients.
They defined extended dosing as any interval from 31 days up to 61 days. They further subdivided the extended dosing patients into those with early extended dosing and late extended dosing. Another 309 patients had dosing that varied and could not be classified into either of those groups.
Patients in the extended dosing groups were at somewhat higher risk for PML than those treated at the recommended interval, with a higher proportion testing positive for JC virus, more patients with a history of immunosuppressant therapy (18 per cent versus 11 per cent), and more total Tysabri doses (mean 39 versus 30). Patient age, disease duration, and gender balance did not differ markedly between standard and extended dosing groups, however.
Among extended dosing patients, the mean duration of that schedule was 23 months overall. These varied only modestly between the early, late, and variable dosing regimens.
Treatment efficacy (Tysabri 's forte) was excellent irrespective of dosing interval. Some 65 per cent of standard and 65 per cent of extended dosing groups showed no evidence of disease activity (NEDA). That is, no active MRI lesions and no clinical activity. The variable extended dosing group suffered a little bit in this respect, with 55 per cent meeting the NEDA standard compared with about 70 per cent for both early and late dosing.
Weinshenker commented that selection of patients for extended dosing, which was not random, might have involved "biases against committing more aggressive MS patients on the extended interval program, which might reduce the ability of the investigators to detect reduction in efficacy."
Nevertheless, he said, extended dosing "is a promising and sensible approach that might turn out to be effective."
Zhovtis-Ryerson and colleagues have established a registry called EXTEND to which other clinicians may contribute, at www.msbase.org. They are also planning a prospective study to examine effects of the different regimens on disability progression over time.
The study had no external funding and authors declared they had no financial interests relevant to the work.
Source: Medpage Today © Medpage Today 2015 (23/04/15)
Although the number of paediatric patients with multiple sclerosis has increased over the years, researchers recently revealed one of the first studies to offer population-based information.
Data from the Paediatric Health Information System (PHIS) has been presented at the 2015 annual meeting of the American Academy of Neurology in Washington, DC. Lead author Amy M. Lavery, MSPH, and her Department of child neurology in the Children’s Hospital of Philadelphia colleagues worked to shed light on a subject that doesn’t have a firm backing of research results.
The authors wrote that since “literature is lacking with respect to overall disease” when it comes to paediatric MS, it was time to “examine the prevalence of hospital admissions.”
From 2004 to 2013, the database revealed inpatient visits, emergency department encounters, and charges encountered from 44 children’s hospitals in the United States. The findings showed a trend in hospital visits among the affected children.
The 1,422 patients – made up of twice as many females – found in the database collectively had 2,068 hospital encounters and stayed for an average of 4 days. In 2004 paediatrics MS patients checked into the hospital an average of 2.37 times, however, that number jumped to 4.13 in 2013. Also, for every 10,000 hospital check-ins the cause associating with MS has increased from 3.47 to 5.95. The reason behind the rate surge, the authors noted, could be attributed to the addition of paediatric MS centres and awareness.
“A test for trend showed a steady, significant increase in encounters for MS,” the team said, which raises the question if that number will continue to grow. For children ages 11 and younger, the amount of MS cases has stayed the same while ages 11 to 15 and 15 and older has steadily increased. This study may be one of the first to address paediatric MS hospitalisations, however, it won’t be the last.
“Further analyses will incorporate pharmacy data and investigate factors contributing to healthcare utilization and hospital admission rates,” the study concluded.
Source: MS All Specialities Copyright HCPLive 2006-2015 Intellisphere, LLC (23/04/15)
MRI patterns decipher between MS and VWM(23/04/15)
Researchers say they have found evidence that makes it easier to differentiate between multiple sclerosis (MS) and vanishing white matter disease (VWM) – conditions that can show considerable similarities.
According to a presentation at the American Academy of Neurology in Washington, DC, diagnosing primary and secondary progressive multiple already presents a challenge because the signs – like large and confluent lesions and multiple cavitary lesions – are rarely shown on a brain MRI. However, the comparable symptoms with VRM can cause a misdiagnosis.
“It is important to identify specific MRI findings that can be relevant diagnostic tools,” the study’s authors wrote.
Lead author Xavier Ayrignac, of the Department of Neurology in Centre Hospitalier Universitaire de Montpellier in France, and his colleagues evaluated 14 MS and 14 VWM patients to find key differences between their brain scans.
“In this context, the diagnosis of multiple sclerosis can be difficult and a diagnosis of VWM should be considered,” Ayrignac and his team determined.
When cavitary lesions show up on the MRI, it becomes more challenging to decipher between the central nervous system diseases. The researchers focused on specific features including regional atrophy, white matter and gray matter hyperintensities location and type, and posterior fossa involvement along with middle cerebellar peduncle and cerebellar white matter lesions.
While similar results were indicated between the MS and VWM patients – like focal atrophy, basal ganglia atrophy, and corpus callosum atrophy – the investigators found important individualized characteristics for the diseases:
- Cerebellum atrophy: 8 (57%) MS patients, 13 (93%) VWM patients
- Topography of the lesions (thalamus): 10 (71%) MS patients, 1 (7%) VWM patients
- Topography of the lesions (midbrain): 11 (79%) MS patients, 4 (29%) VWM patients
- Extensive juxtacortical lesions: 7 (50%) MS patients, 14 (100%) VWM patients
- Ovoid perpendicular to the ventricle: 14 (100%) MS patients, 0 VWM patients
- Corpus callosum extensive: 9 (64%) MS patients, 14 (100%) VWM patients
- Extensive lesions (external capsule): 4 (29%) MS patients, 12 (86%) VWM patients
- Perivascular cavitary lesions: 10/12 (83%) MS patients, 1/6 (17%) VWM patients
- Infratentorial symmetrical: 0 MS patients, 6/12 (50%) VWM patients
- Fluid like cavitary lesions: 3 (21%) MS patients, 9 (64%) VWM patients
“Nevertheless, our results suggest that the analysis of characteristics of MRI findings including topography and morphology of the lesions is of major diagnosis importance for the differential diagnosis of these 2 disorders,” the team concluded.
Source: MD All Specialities Copyright HCPLive 2006-2015 Intellisphere, LLC (23/04/15)
In a new study, researchers have made insights into how the blood-brain barrier (BBB) - which allows only selected molecules to pass through - is maintained, identifying a protein key to the process. Delivering this protein to mice with the rodent equivalent of MS improved their symptoms.
In certain diseases, however, such as multiple sclerosis, the barrier can be improperly breached. These "leaks" can allow immune cells and inflammatory molecules to pass through, causing inflammation that leads to neuronal damage.
The research, led by the University of Pennsylvania's Jorge Ivan Álvarez and Cornelia Podjaski of McGill University and Alexandre Prat of the University of Montreal, will appear in the journal Brain.
Alvarez, an assistant professor in Penn's School of Veterinary Medicine, conducted the study with Podjaski and Prat and colleagues from McGill University and from the University of Montreal.
In 2011, Alvarez and Prat published a study in Science that showed that the protein sonic hedgehog, or Shh, is secreted by central nervous system cells called astrocytes and plays a key role in blood-brain barrier maintenance, in part by preventing immune cells from entering the brain. But the researchers still didn't have a complete picture of the signaling events downstream of Shh that mediated this effect. To learn more, they first used human cells in culture from the blood-brain barrier, called endothelial cells. They found that applying Shh to the cells caused levels of a protein called netrin-1 to rise.
In mice bred to lack the molecular receptor for Shh, netrin-1 expression was reduced, indicating that netrin-1 expression depends on Shh.
"Netrins are best known to play a role in guiding the direction of axon growth as well as morphogenesis and tissue formation," Álvarez said. "But our work suggested a new role for netrin-1 in the blood brain barrier."
Curious as to whether this might influence MS, they examined BBB cells from the brains of people who had died from the disease. Normal tissue from these individuals contained low levels of netrin-1, while the diseased lesions in the brain had higher levels. The researchers found similar results in a mouse model of MS called experimental autoimmune encephalomyelitis, or EAE.
Next, the team directly measured netrin-1's effect on BBB permeability by labeling tracer molecules and found that netrin-1 significantly reduced the movement of molecules across cultures of human BBB endothelial cells. Further experiments showed that netrin regulates this process by promoting the expression of the so-called "tight junction" proteins, which are located between BBB endothelial cells and are responsible for controlling barrier function. The team also found that, when in an environment rife with inflammatory signaling molecules, which would normally compromise the integrity of the BBB, netrin-1 had a counteracting effect, preventing disruption to the BBB.
"In mice bred to lack netrin-1, we observed that proteins normally found in the blood accumulated in the animals' brain, another sign that netrin-1 ensured the integrity of the BBB," Podjaski said.
Armed with these findings suggesting netrin-1 protects the BBB, the team tested the potential of netrin-1 in ameliorating EAE symptoms, which are similar to those of people with MS.
"By administering netrin-1 to mice before the EAE disease was induced, we found that animals had less severe disease, delayed disease onset, fewer lesions in their brain, fewer markers of inflammation and better maintenance of body weight compared to mice given a sham treatment," Podjaski said.
"In mice, we found the disease outcome is better when they're treated with netrin-1, even when delivered after disease processes had begun," Alvarez said. "And all those observations held up in vitro as well."
Moving forward, the researchers hope to further elucidate the pathway through which Shh and netrin-1 operate, with an aim toward finding more effective ways to uphold the barrier and perhaps one day treat diseases like MS.
"We now know that Sonic is above netrin-1 in the signaling pathway, but what else is Sonic hedgehog doing?" Prat said. "We need to complete the puzzle with Sonic first to give us better therapeutic strategies."
Source: Source: Medical Xpress © Medical Xpress 2011-2015, Science X network (23/04/15)
Acorda Therapeutics Inc has presented data from a Phase 1 clinical trial of rHIgM22, a remyelinating antibody being studied for the treatment of multiple sclerosis.
Safety data showed rHIgM22 was well-tolerated in each of the five tested doses, supporting additional clinical development. In addition, testing detected rHIgM22 in cerebrospinal fluid (CSF), indicating the drug’s access to the central nervous system.
These data were presented at the 67th American Academy of Neurology Annual Meeting in Washington, DC.
“In this study, rHIgM22 was well-tolerated over the full range of dose levels tested. Furthermore, we were able to verify that rHIgM22 is present in the CSF, showing that the antibody is available to the brain,” said Anthony Caggiano, M.D., Ph.D., Acorda’s Senior Vice President of Research and Development.
“We plan to advance our clinical program based on this data. The next study will include patients experiencing acute relapses. The combined results of these two studies will inform subsequent trials, which we anticipate will enrol both stable patients and those experiencing active relapses.”
This was a placebo-controlled, single-dose, escalating study in 72 patients with clinically stable MS to explore dose tolerability for six months after treatment. rHIgM22 was well-tolerated at all doses tested, with no safety signals identified. There were no dose-limiting toxicities and no serious adverse events in any of the five rHIgM22 dose levels in the study. The data presented included the concentration of rHIgM22 in the CSF at two days and four weeks after IV infusion. The antibody was measured at levels expected for antibodies of this class. There were no significant changes from baseline in clinical measures including MRI, magnetic resonance spectroscopy, Expanded Disability Status Scale, Timed 25-Foot Walk, and low contrast visual acuity.
The most commonly observed adverse events (>5% in the combined rHIgM22 treatment groups) reported in the study were: headache, contact dermatitis, multiple sclerosis relapse, infusion site hematoma, fatigue, arthralgia, back pain, muscular weakness, neck pain, pain in an extremity, pruritus, contusion, and flushing. No participants withdrew due to adverse events. No safety signals were identified by standard clinical MRI evaluations, or standard clinical, laboratory or ECG assessments.
Source: Finances © 2014 Finances International Ltd (23/04/15)
Doctor offers new model for MS(22/04/15)
Multiple sclerosis may be more of a continuum than three distinct types of disease, and a new model attempts to capture that nuance reports MedPage Today.
The "topographical" model could provide a new way of looking at disease course, Stephen Krieger, MD, of Mount Sinai in New York City, claims.
"There's thought that MS is more of a continuum," Dr Krieger said.
"We should not think in terms of those categories, but we should think of it as a mixture of relapses and progression and how specifically they mix together."
Currently, MS is classified as being in one of three groups: relapsing-remitting, secondary progressive, and primary progressive. But Dr Krieger, a protege of Fred Lublin, MD, who created the three-category model, said the system doesn't accurately capture the range of disease.
"There's real diagnostic uncertainty," Dr Krieger told MedPage Today.
"It takes us years to figure out which category someone is in. A lot of progressive patients stay like they are for years. You're not always sure which category someone fits into, nor do those categories tell us how someone's disease is going to progress."
For his new model, which Dr Krieger calls a "true admixture of inflammation and progression" that describes the clinical course of MS in a more biologically informed way, he incorporated five factors: topographical distribution of lesions and the relapses they cause, relapse frequency, relapse severity, relapse recovery, and progression rate.
It essentially suggests the clinical manifestations of MS are a consequence of the interplay between inflammatory lesions - the relapsing part of the disease - and generalised loss of functional capacity, as seen in the progressive part of the disease.
To illustrate the concept, Dr Krieger came up with a peak-and-pool model. There's a shallow end that drops off into a deep end, where the shallow end represents the spinal cord and optic nerve, the mid-section represents the posterior fossa, and the cerebral hemispheres constitute the deep end.
At the same time, brain lesions appear as topographic peaks that rise from the floor of the pool. The water's surface is the clinical threshold, and when the central nervous system lesions' peaks cross it, a relapse or flare occurs.
Disease progression is represented by a falling water level, which essentially represents a loss of neurons and declining brain volume, something that can be measured on MRI, Dr Krieger said. The model also implies progression could take the form of relapses as these peaks start to rise above the water, Krieger said.
The very visual disease representation was the result of a pro bono collaboration with Harrison and Star, a healthcare communications company.
When asked what his mentor Lublin thought about the challenge to his work, Dr Krieger said he's been "incredibly supportive."
"He thinks it's really interesting, and he wants to see me make it into an applied model for prediction," Dr Krieger said.
"We'll try to operationalise it over the coming couple of years and figure out how to do precise metrics. We'll figure out how to take a clinical trial database and apply that and figure out things we otherwise couldn't."
Source: MedPage Today © 2015 MedPage Today, LLC (22/04/15)
A new study by the NYU Langone Medical Centre found almost 40 per cent of patients had some disease activity return when they stopped taking their meds. The findings, issued in a press release by the centre, have been presented at the American Academy of Neurology Annual Meeting held April 18-25, in Washington, D.C.
"Despite long periods of disease stability while taking medication, we found a large minority of patients who stopped experienced relapses or disability progression," said lead study author Ilya Kister, MD, an assistant professor of neurology at the NYU Langone Multiple Sclerosis Comprehensive Care Center.
"We need to identify situations when it is safe for patients with MS to stop taking these medications."
Little is known about MS disease progression after first-line, disease-modifying therapies are discontinued in clinically-stable patients.
For the study, Dr. Kister and colleagues prospectively studied 181 patients from the global observational MSBase Registry, examining MS relapse rates and disability progression rates in patients who stopped taking disease-modifying therapy.
Patients in the study were aged 40 and older, had experienced no relapses and reported stable disability progression (measured by EDSS scores) for at least 5 years, and had been taking medication for at least three years. Once medications were ceased, patients were followed for at least three years.
After discontinuing medication, 24 per cent of patients experienced a clinician-reported relapse, 32 per cent sustained three-month disability progression, and 10.6 per cent of patients recorded both relapses and disability progression.
Researchers found 77 patients - or 42 per cent - restarted medication after an average of 22 months. Restarting medication was associated with a 59 per cent risk reduction of disability progression.
"Decisions regarding stopping disease-modifying therapy may have implications for short and long-term prognosis. We know a lot about what happens when therapy is started, but we know very little about what happens when therapy is stopped", said Dr Kister.
Dr Kister and colleagues are now calling for a randomised trial of discontinuation of disease-modifying therapy to provide more evidence of when exactly it might be safe for patients to stop taking their medications.
Source: EurekaAlert! Copyright © 2015 by the American Association for the Advancement of Science (AAAS) (22/04/15)
According to study results presented at the 2015 annual meeting of the American Academy of Neurology in Washington, DC, researchers say they have tied the effects of cigarette smoke with various health issues experienced by current and potential multiple sclerosis patients.
“In previous studies we demonstrated that rats exposed to cigarette smoke develop increased brain inflammation and oxidative stress,” lead author Walter Royal III, MD, and colleagues wrote in the presentation. “In these studies we examine the effects of cigarette smoke exposure on systemic and brain inflammatory responses in a murine model of MS, experimental allergic encephalomyelitis (EAE).”
The team analysed female mice under different conditions by splitting them up into one of the following groups:
Exposed to the smoke chamber but not cigarette smoke or induced to get EAE
Exposed to cigarette smoke but not induced to get EAE
Not exposed to cigarette smoke but induced to get EAE
Exposed to cigarette smoke and induced to get EAE
Not exposed to cigarette smoke or the smoking chamber (controlled group)
For the mice that were exposed to cigarette smoke (5 days per week for 4 weeks) the cigarettes contained the “regular” amount of nicotine (0.7 mg per stick and tar (9.4 mg per stick). Also, they were restrained and ventilated by the smoke machine. The mice were immunized with oligodendrocyte glycoprotein peptide fragment after one month of cigarette smoke exposure and after an additional two weeks their brains were removed for further evaluation.
The authors noted that the control group was under the same restraints but without the smoke.
From this examination the team found that in the mice induced to develop EAE, the ones who were also exposed to cigarette smoke had “significantly enhanced pro-inflammatory response, with increased levels of immune cell activation and cytokine secretion.” The smoke was associated with higher oxidative stress, as previous studies have suggested, and lower expression of Nrf2 as well. The researchers pointed out that in the mice with EAE exposed to cigarette smoke, the nuclear translocation of the transcription factor climbed.
“Such effects may contribute to the development of enhanced disease activity among individuals with MS, and, therefore, studies of the mechanisms and potential treatment of these effects are required the authors wrote.
The study authors concluded that cigarette smoke increases the risk of developing the disease while also making it more likely that treatment will fail.
Source: MD All Specialities Copyright HCPLive 2006-2015 Intellisphere, LLC (22/04/15)
Three year data on Plegridy revealed (22/04/15)
Biogen has announced new data from the ATTAIN study which demonstrate the long-term safety and efficacy of Plegridy over a three-year period in people with relapsing-remitting multiple sclerosis (RRMS). The interim results from the first year of ATTAIN, a two-year extension study of the Phase 3 study, show the benefits of continued Plegridy treatment on clinical outcomes and further define its safety profile.
“This data offers additional insights into the benefit-risk profile of Plegridy by demonstrating a consistent safety profile and continued efficacy over three years,” said Bruce Hughes, M.D., director of the Ruan Multiple Sclerosis Center at Mercy Ruan Neurology Clinic and Research Center in Iowa.
“Long-term safety and robust efficacy are important considerations when evaluating treatment options for this chronic condition.”
The most common side effects reported were injection site reactions and flu-like symptoms, the majority of which were mild or moderate. The rate of neutralizing antibodies was one percent after three years.
Source: Finances © 2015 Finances International Ltd (22/04/15)
Scientists in Australia have made an important discovery about spider venom that could lead to a new class of painkillers.
Spiders use their venom to immobilize or kill their prey. Researchers from the University of Queensland isolated seven peptides—the building blocks of proteins—in spider venom that blocked the molecular pathway responsible for sending pain signals from the nerves to the brain. One peptide in particular, from a Borneo orange-fringed tarantula, had the right structure, stability and potency to potentially become a painkilling drug, the researchers said. The study was recently published in the British Journal of Pharmacology.
The medical community is eager to identify new medications to treat chronic pain, which affects about 15 per cent of all adults, according to a 2012 study published in the Journal of Pain. Traditional painkillers such as morphine and widely used medications like hydrocodone can be addictive, and abuse of the drugs has soared in recent years, prompting stricter regulations from the U.S. Drug Enforcement Administration.
“Spider venom acts in a different way to standard painkillers,” said Jennifer Smith, a research officer at the University of Queensland’s Institute for Molecular Bioscience. Dr. Smith, one of the authors of the Australian study, doesn’t expect a painkiller derived from the venom will be addictive because it blocks a specific channel that transmits pain to the brain. Opiate painkillers, by contrast, block widespread opioid receptors on cells in the brain, spinal cord and other organs.
Spiders aren’t the only venomous creatures with medicinal potential. Researchers in France have found ingredients in the venom from Africa’s black mamba snake, one of the world’s deadliest, had painkilling properties as potent as morphine. And a drug derived from the venom of the sun anemone, which lives on reefs in the Caribbean, is currently being tested in the U.S. on people with psoriasis and could also be used to treat other autoimmune disorders such as multiple sclerosis and rheumatoid arthritis.
Scientific interest in venom’s painkilling properties stems from an earlier discovery by geneticists of a rare mutation in some people—in a gene known as SCN9A—that eliminates their ability to feel pain. While they can experience touch, warmth and other tactile functions, their sense of smell and pain are inhibited, Dr. Smith said. Some venoms from spiders and other animals and plants have been found to mimic the effects of the gene mutation.
The Australian study analysed spider venom from 205 species found locally and in other countries (there are currently about 45,000 known species of spiders in the world). The researchers isolated various active peptides from the venom. Each peptide was studied to see how it would affect specific pain targets known as ion channels, which transmit pain signals through the body.
About 40 per cent of the tested spider species contained at least one peptide that blocked pain channels. The researchers plan to conduct animal studies to test the peptides’ clinical potential, looking for any unforeseen side effects, whether the substances break down in the body and other outcomes, Dr. Smith said.
“We’ve got a massive library of different venoms from different spider species and we’re branching out into other arachnids: scorpions, centipedes and even assassin bugs,” Dr. Smith said.
Some, such as the Sydney funnel-web spider, a native to Australia, were easy to milk because they are very aggressive. “Literally, you have to just look at them and they’ll start dripping venom from their fangs,” Dr. Smith said. The spider’s venom, however, didn’t contain ingredients capable of blocking pain channels, she said.
Others, including South American tarantulas the size of dinner plates, had to be anesthetized and the muscles around the venom gland stimulated for venom to be produced, she said. A university researcher traveled the world to collect venoms from spiders kept by arachnid enthusiasts and pet shops.
Australia is a natural fit for this research, Dr. Smith said. “We have a plethora of really good venomous animals: You name it we’ve got it, pretty much. Australia is the venom land.”
The Australian research is funded in part by Janssen Pharmaceuticals Inc., a unit of Johnson & Johnson. “We think this is scientifically promising, but it is too early to put time frames around when this might be in the clinic or a product would be available,” a Janssen spokesman said.
Experiments with the black mamba snake also aim to develop nonaddictive painkillers. The snake, which has olive-gray skin and can grow as long as 12 feet, gets its name from the color inside its mouth, which it displays when threatened.
Researchers at France’s National Center for Scientific Research tested peptides from the black mamba snake’s venom called mambalgins on mice and found potent painkilling properties. The peptides focused on a different pain pathway than the opioid receptors targeted by morphine, according to the research, published in the journal Nature in 2012.
Venom from the sun anemone is being developed into a drug called dalazatide by Seattle-based biotech company Kineta Inc. A human clinical trial with the drug as a treatment for psoriasis recently concluded and results are expected to be released in the next few weeks, according to Kineta. Unlike traditional treatments for autoimmune disorders that suppress the entire immune system, Kineta’s drug is intended to block only the white blood cells that cause the diseases, said company chief executive Charles Magness.
Source: The Wall Street Journal Copyright ©2015 Dow Jones & Company, Inc (21/04/15)
In a study of 1,964 patients with multiple sclerosis, researchers at the NYU Langone Multiple Sclerosis Comprehensive Care Center found that extending the dose of natalizumab from four weeks up to eight weeks was shown to be well-tolerated and effective in patients, and resulted in no cases of the potentially fatal side effect progressive multifocal leukoencephalopathy (PML).
The drug showed similar efficacy in treating disease activity among patients, according to the study led by Lana Zhovtis-Ryerson, MD, an assistant professor of neurology at the NYU Langone Multiple Sclerosis Comprehensive Care Center.
Natalizumab is an infusion drug known as a monoclonal antibody that is used to prevent MS symptoms and flare-ups and slow worsening disability.
However, taking the medication for longer than two years may increase risk for a rare but potentially fatal side effect called PML, an untreatable brain infection that occurs in up to 1.3 percent of patients taking natalizumab.
The medication is typically prescribed in 300-milligram infusions every four weeks.
"There remains much unknown about whether the drug will lose effectiveness if dosing is extended," explains Dr. Zhovtis-Ryerson. "Our study showed treatment with natalizumab was safe for patients with similar efficacy reported as the standard dosing, potentially enabling patients to stay on effective MS medication at a reduced frequency of infusions and with lower risk of PML. "
Zhotvis-Ryerson and colleagues at 10 American MS. Centers sought to compare the safety and efficacy of an extended dose of natalizumab to the standard dose. They retrospectively compared 1,078 patients taking a standard 4-week dose to 886 taking an extended dose between 4 weeks, 3 days and 8 weeks, 5 days.
The researchers found extending the dosing schedule of natalizumab to between 5 and 8 weeks does not affect the drug's efficacy profile with 65 per cent of participants in each group not showing clinical MS activity, and comparable rates of new lesions reported on imaging. Zero cases of PML were reported in the extended dosing group, while two cases were reported in the standard dose group, though the researchers said statistical significance has not been reached yet. No other major adverse events were reported.
"While the findings are encouraging, more research is needed to determine whether extending natalizumab dosing may reduce disability progression," says Dr. Zhovtis-Ryerson.
Natalizumab is manufactured by Biogen and Elan, and sold under the name Tysabri.
Source: MedicalXpress © Medical Xpress 2011-2015, Science X network (21/04/15)
Mindfulness-based cognitive therapy may be as good as pills at stopping people relapsing after recovering from major bouts of depression, according to a new study.
Mindfulness-based cognitive therapy (MBCT) was developed from mindfulness techniques, which encourage individuals to pay more attention to the present moment, combined with cognitive behaviour therapy (CBT), specifically to try to help people who have recurring depression.
It teaches people to recognise that negative thoughts and feelings will return, but that they can disengage from them.
The trial, published in The Lancet involved a group of 424 adults from GP practices in the south-west of England, who were willing to try either the pills or the therapy. Half were randomly allotted to each. Those assigned to mindfulness had eight group sessions of more than two hours plus daily home practice and the option of four follow-up sessions over a year. The course involved mindfulness training, group discussion and cognitive behaviour exercises. The patients gradually came off their medication. Those assigned to the other group stayed on the tablets for two years.
The relapse rates in the two groups were similar, with 44% in the mindfulness group and 47% for those on the drugs. In each group there were five adverse events, including two deaths.
The researchers had thought the study might show that therapy was more effective than pills, based on their earlier work. Lead author Willem Kuyken, a professor of clinical psychology at the University of Oxford, said: “That was our hypothesis. It was based on our pilot study in 2008. There was a suggestion that MBCT might do better than medication. The reality is that it was not superior to medication.”
However, they established that mindfulness-based therapy is equally as good as drugs, which could offer a new option for those who do not want to be on medication for years. Co-author Prof Richard Byng, from the Plymouth University Peninsula Schools of Medicine and Dentistry, said: “Currently, maintenance antidepressant medication is the key treatment for preventing relapse, reducing the likelihood of relapse or recurrence by up to two-thirds when taken correctly.
“However, there are many people who, for a number of different reasons, are unable to keep on a course of medication for depression. Moreover, many people do not wish to remain on medication for indefinite periods, or cannot tolerate its side-effects.”
Nigel Reed, from Sidmouth, Devon, who took part in the trial, said: “Mindfulness gives me a set of skills which I use to keep well in the long term. Rather than relying on the continuing use of antidepressants, mindfulness puts me in charge, allowing me to take control of my own future, to spot when I am at risk and to make the changes I need to stay well.”
The study also showed that the therapy might work better than pills for those who have some of the most troubled histories and are at the highest risk of relapse. It was found to have protected people with increased risk because of a background of childhood abuse. The paper said: “Perhaps MBCT confers resilience in this group at highest risk because patients learn skills that address some of the underlying mechanisms of relapse or recurrence.”
Kuyken said he expected Nice to look at the study when it convenes shortly to revise its guidelines on recurrent depression.
Source: The Guardian © 2015 Guardian News and Media Limited (21/04/15)
A common athlete’s foot cream sold over the counter at most chemists could help people living with multiple sclerosis, a new study claims.
Researchers believe the drug miconazole - the active ingredient in Daktarin - instructs stem cells in the brain to repair nerve damage. The discovery comes after a team at Case Western Reserve University in Ohio tested more than 700 drugs to see if anyone would be useful against MS.
The athlete’s foot drug and a cream used to treat eczema were found to stimulate the regeneration of damaged brain cells. It was found to reverse paralysis in mice.
"We know that there are stem cells throughout the adult nervous system that are capable of repairing the damage caused by multiple sclerosis, but until now we had no way to direct them to act," said Dr Paul Tesar, Professor of Innovative Therapeutics at Case Western Reserve School of Medicine.
"Our approach was to find drugs that could catalyse the body's own stem cells to replace the cells lost in multiple sclerosis."
The team said that much work remains before multiple sclerosis patients might benefit from the promising approach.
Scientists still must find ways to transform the medications for internal use and determine their long-term efficacy and potential side effects.
However they said the initial findings show promise and the drugs have been shown to work on human stem cells.
“This truly represents a paradigm shift in how we think about restoring function to multiple sclerosis patients,” said Dr Robert Miller of the neurosciences faculty.
"The drugs we identified are able to enhance the regenerative capacity of stem cells in the adult nervous system. It showed a striking reversal of disease severity in the mice.”
The research was published in the journal Nature.
Source: The Daily Telegraph © Copyright of Telegraph Media Group Limited 2015 (21/04/15)
Medical professionals have been urged to consider a wide range of possible symptoms when it comes to neurological conditions such as multiple sclerosis.
The move comes after a case where a seven-year-old boy's only symptoms were abdominal pains.
According to the study 'Acute Abdominal Pain As The Only Symptom Of A Thoracic Demyelinating Lesion In Multiple Sclerosis', published in the journal Brain And Development, the child had a new demyelinating lesion that showed up on his spine.
The boy had his first MS symptom at the age of three. At that time, he had spastic gait and was treated with intravenous methylprednisolone (m-PSL). Although he continued to have slight spasticity in both his ankle joints, his symptoms were greatly improved.
Later, at the age of six, the boy had a second MS symptom. He appeared at the doctor due to neck and upper extremity pain and was diagnosed with multiple sclerosis. A more aggressive means of treatment included interferon-beta 1a (IFN β 1a) and plasmapheresis in addition to m-PSL. Treatment with IFN β 1a was stopped because the boy had frequent episodes of vomiting and poor eating, both of which cleared up one month after stopping IFN β 1a treatment.
With the newest relapse, the boy was treated again with m-PSL and IFN β 1b (rather than IFN β 1a). Remarkably, there was a reduction in the demyelinating lesion with the end of treatment, as well as a resolution of symptoms after three weeks.
“This case is remarkable in that the only symptom of a longitudinally extensive, thoracic, demyelinating lesion was abdominal pain,” said Dr. Shohei Nomura, lead author of the case study.
“Though it is unclear why the only manifestation of this patient’s extensive thoracic lesion was abdominal pain, this case supports the notion that the size and localization of demyelinating lesions might not directly correspond to the symptoms observed. Therefore, clinicians must be careful to consider neurogenic sources of diverse symptoms, especially those related to autonomic dysfunction, in demyelinating diseases such as multiple sclerosis.”
Source: Multiple Sclerosis News Today © BioNews Services 2015 (20/04/15)
Biogen announces latest Tecfidera data(20/04/15)
Biogen has announced new data that continues to support Tecfidera as an effective, long-term treatment for people who are living with relapsing-remitting multiple sclerosis (RRMS).
Data shows Tecfidera significantly reduced relapses and disability progression in newly-diagnosed RRMS patients who had highly active forms of the condition. Additional data indicates Tecfidera showed strong and sustained efficacy over five years in RRMS patients who were previously treated with an interferon or glatiramer acetate (GA).
“Taken together, these studies reinforce that Tecfidera delivers robust efficacy when used as a first-line therapy, as well as when it is used after a patient has discontinued interferon or glatiramer acetate treatment,” said J. Theodore Phillips, M.D., Ph.D., research investigator at the Baylor Institute for Immunology Research and clinical professor of Neurology at the University of Texas Southwestern Medical Center.
“In addition, strong efficacy was observed with Tecfidera treatment in various patient populations including those with highly active MS.”
In 2014, emaxheath.com reported that more than half of patients taking Tecfidera required over-the-counter medications to try and manage side effects such as vomiting and diarrhea. The site also reported that 25 per cent of patients who switched to Tecfidera from another MS treatment stopped taking the drug within three months.
A study by the University Of California also found that, in a study group of 30 patients, five stopped taking the drug because of gastrointestinal side effects, 13 reported significant side effects while 12 said they'd had minimal or no side effects.
Source: Street Insider.com © Copyright 2015 StreetInsider.com (20/04/15)
Drug succeeds in trial(17/04/15)
An experimental drug comprising of a high-dose formulation of the food additive biotin has successfully helped patients with primary and secondary progressive MS in a major clinical trial, its French maker claims.
Biotin, also known as vitamin H, is already an approved food additive but the pharmaceutical-grade dose used in biotech company MedDay's drug MD1003 is 300 mg a day, which is 10,000 times the recommended daily food intake.
MedDay said a Phase III study with MD1003 met its goal of improving disability scores in patients after nine months and one year of treatment, potentially paving the way for the medicine to reach the market next year.
If all goes to plan, MedDay's drug could reach the market ahead of rival products in development at other companies, including Biogen's BII033, which is currently in Phase II clinical testing.
Although biotin is not a newly invented chemical, MedDay has U.S. and European patents protecting the dose and its use for MS.
Source: Reuters © Thomson Reuters 2015 (17/04/15)
The Food and Drug Administration has approved the first-ever generic version of the multiple sclerosis drug, Copaxone, which was developed by Momenta Pharmaceuticals. However, it’s still unclear when the drug might become available to patients.
Momenta developed the drug, to be marketed under the name Glatopa, in partnership with New Jersey-based generics company, Sandoz.
The original drug of which Glatopa is a generic version, called Copaxone, is marketed by Israeli drug firm Teva Pharmaceuticals and generated more than $4bn in revenue last year.
Momenta’s attempts to get approval of Glatopa have been tied up in patent battles with Teva. A statement from Momanta says only that Sandoz “is currently evaluating launch timing.”
Source: Boston Business Journal © 2015 American City Business Journals. (17/04/15)
National Theatre Assisted Performances(17/04/15)
The National Theatre has released the latest season listings for Assisted Performances at the National Theatre, through to July 2015. Some productions are provided with Audio-described performances and touch tours for Blind and visually impaired people, Captioned performances for deaf or partially hearing visitors and Relaxed performances are aimed at anyone who would benefit from a more relaxed performance environment including people with an Autistic Spectrum Condition, sensory or communication disorders, or a learning disability.
More information about Accessibility at the National Theatre, and individual listings of performances can be found here: http://www.nationaltheatre.org.uk/your-visit/access
Source: The National Theatre 917/04/15)
A three-week study by Biogen and the American patient network PatientsLikeMe claims to have found patients with multiple sclerosis can benefit from a wearable device that tracks their activity, reports the Boston Business Journal.
Biogen and the patient platform, which collects and shares patient experiences on its website, conducted the study to show the feasibility of using wearables.
“MS impairs the ability to walk for many people with MS, yet we only assess walking ability in the limited time a patient is in the doctor’s office,” said Dr. Richard Rudick, vice president of value-based medicine at Biogen.
“Consumer devices can measure number of steps, distance walked, and sleep quality on a continuous basis in a person’s home environment. These data could provide potentially important information to supplement office visit exams.”
The study found patients were receptive to wearing a device and sharing their data, and said the device helped prompt patients to be more active and helped them manage their MS.
Of the 248 PatientsLikeMe members who were provided with activity trackers, 213 activated the device and authorized PatientsLikeMe to access their data. Another 203 tracked data on the device.
Source: Boston Business Journal © 2015 American City Business Journals (15/04/15)
New drug could reverse MS damage(15/04/15)
A new experimental drug, anti-LINGO-1, has been found to repair myelin and so radically improving nerve signalling, reports The Daily Telegraph.
The scientists studied patients who had optic neuritis – damage of the optic nerve.
The results showed 53 per cent of people on the drug saw their nerve signalling restored to normal or nearly normal while on average most saw signalling between the retina and the brain improve by 41 per cent.
Although the subjects tested were not actually diagnosed with multiple sclerosis, scientists say the new results prove anti-LINGO-1 can repair myelin, and so could help people with MS.
"This study, for the first time, provides biological evidence of repair of damaged myelin in the human brain, and advances the field of neuro-reparative therapies," said study lead author Dr Diego Cadavid, of Biogen.
All patients involved in the trial were given the new drug or a placebo once every four weeks for a total of six doses.
Because optic neuritis only usually affects one eye, doctors evaluated the recovery of the optic nerve by comparing it with the normal healthy eye.
The scientists are now following up patients to find out of the signalling improvement will restored their vision.
"More studies are needed to evaluate whether these changes lead to clinical improvement," said Cadavid.
The drug works by targeting ‘Lingo-1’ a protein which stops nerve cells from developing further once the nervous system is fully formed.
By blocking that protein, the drug effectively tells the body to carry on growing the nerves, which repairs any damage.
Biogen chief medical officer Alfred Sandrock said “We believe the results are encouraging, as this is the first clinical trial to provide evidence of biological repair in the central nervous system by facilitating remyelination following an acute inflammatory injury”.
Source: The Daily Telegraph © Copyright of Telegraph Media Group Limited 2015 (15/04/15)
A Canadian study has found no link between the delayed onset of secondary progressive multiple sclerosis and treatment with beta-interferons.
In the study, Beta-interferon Exposure And Onset Of Secondary Progressive Multiple Sclerosis, published in the European Journal Of Neurology, the researchers set out to examine the association between beta-interferons and the onset of secondary progressive MS in patients with relapsing-remitting MS.
Beta-interferons are the most widely prescribed drugs for patients with MS, but whether or not treatment with beta-interferons can delay the onset of secondary progressive MS onset has always been unclear.
The scientists took 794 patients with relapsing-remitting MS and compared them with a healthy control group. The outcome was gauged from the start of treatment with beta-interferons to confirmation of the onset of secondary-progressive MS.
In the published results, the researchers reported: “The median follow-up for the beta-interferon-treated, untreated contemporary and historical controls were 5.7, 3.7 and 7.3 years, and the proportions of patients reaching secondary progressive MS were 9.2 per cent, 11.8 per cent and 32.9 per cent, respectively. After adjustment for confounders, beta-interferon exposure was not associated with the risk of reaching secondary progressive MS when either the contemporary or the historical untreated cohorts were considered.”
The study concluded that, amongst patients with relapsing-remitting MS, use of beta-interferons was not associated with a delayed onset of secondary progressive MS.
Source: Eur J Neurol. 2015 Apr 6. doi: 10.1111/ene.12698. & PMID: 25846809 (13/04/15)
PML death linked to Tecfidera(10/04/15)
The brain infection progressive multifocal leukoencephalopathy (PML) has killed a Dutch psoriasis patient who was taking a high dose of a drug with ingredients similar to Tecfidera. Tecfidera is used for multiple sclerosis, which the Dutch patient didn’t have, and the medicine was made in a compounding pharmacy and not by Biogen. Yet, according to Bloomberg.com, doctors claim the case suggests the infection could emerge in people who aren’t showing warning signs.
The PML infection was detailed in the New England Journal of Medicine, accompanied by a separate report on a multiple sclerosis patient who died of PML while taking Biogen’s drug.
While physicians can monitor patients for signs of PML, the 64-year-old psoriasis patient didn’t have seriously low levels of infection-fighting white blood cells, thought to be an indicator of risk for PML.
The Dutch case is the first found in a person on dimethyl fumarate, the active ingredient in Tecfidera, who didn’t have early warning signs. That’s “a situation previously thought to be unlikely,” wrote Dennis Nieuwkamp and other doctors from the University Medical Center Utrecht, in the Netherlands.
It’s not appropriate to extrapolate the risks of a pharmacy-mixed drug to Tecfidera, said Catherine Falcetti, a Biogen spokeswoman. The pharmacy-made drug containing dimethyl fumarate, called Psorinovo, is an unregulated product and differs from Tecfidera based on the amount and nature of the active substances, as well as the specific formulation and doses, she said.
There has been only one case of PML in a Tecfidera patient, out of more than 135,000 who have received it. Doctors are told to monitor patients’ blood to detect low white cell counts, a known risk for PML, Falcetti said.
Since the number of people getting dimethyl fumarate is rapidly increasing because of Tecfidera, “our case raises important questions with respect to safety monitoring,” the Dutch doctors wrote.
The report isn’t likely to change use of Tecfidera, however, said Karen Blitz, director of the North Shore-LIJ Multiple Sclerosis Center in East Meadow, New York. The drug helps patients remain functional and many are willing to take risks for that benefit, she said. The danger is exceptionally rare, she added. “If there is another case in a patient taking the currently recommended dose of Tecfidera, that would be interesting,” said Blitz. “Unless there is more data indicating a risk, I’m going to continue to use the drug and monitor white blood cell counts.”
Source: Bloomberg Business ©2015 Bloomberg L.P (10/04/15)
America’s National Multiple Sclerosis Society has committed $28m to support an expected 84 new MS research projects and training awards, it has been revealed.
This financial commitment is the latest in the Society's projected investment of over $52m in 2015 to support 380 new and ongoing studies around the world.
Among the research projects are a University of California, San Francisco-led consortium focusing on a comprehensive analysis of the gut microbiome to develop probiotic strategies for stopping progressive MS; a pilot trial at Johns Hopkins University exploring the tolerability of a diet that intermittently restricts calorie intake as a treatment for disease activity in people with MS; pre-clinical studies by a commercial firm (Bionure) to test the potential of a compound to protect the nervous system and stimulate repair of nerve-insulating myelin; and a new collaborative center at Oregon Health & Science University to research patient-centered wellness programs to improve the daily life of people with MS.
"MS research is a top National MS Society priority, with increasing annual investments to drive solutions for every person with MS," said Cyndi Zagieboylo, President and CEO of the Society.
"We fund the entire research spectrum, propelling novel ideas into the lab, translating breakthroughs into clinical trials, and moving success in clinical trials into new treatments for people living with MS."
Source: PR Newswire Copyright © 2015 PR Newswire Association LLC (08/04/15)
MedDay, a biotechnology company focused on the treatment of nervous system disorders, has provided further information about the design of its pivotal clinical trial (MS-SPI) to investigate the efficacy and safety of MD1003 in the treatment of primary and secondary progressive multiple sclerosis.
MS-SPI is a randomised, double-blind, multicenter, placebo-controlled (2:1) trial of MD1003, 300 mg/day, in patients with progressive MS who have demonstrated progression in the two years prior to enrolment.
A total of 154 patients with a baseline EDSS (Expanded Disability Status Scale) score of between 4.5 and 7 were enrolled from 16 MS reference centres across France. Treatment duration was one year.
The primary endpoint for the study was defined as the proportion of patients who improved at nine months (M9), with confirmation at 12 months (M12). Improvement was defined as either a decrease in EDSS or an improvement in TW25 (a timed 25-foot walk) of at least 20 per cent. The comparison for each outcome was the best EDSS and TW25 scores obtained at the screening and randomisation visits.
The main secondary endpoints evaluate the effect of MD1003 in stabilising or slowing down the rate of progression. These endpoints include the change in EDSS between M0 and M12, the proportion of patients with progression at M9 confirmed at M12 and the change in TW25.
Frédéric Sedel, MD, Chief Executive Officer of MedDay, said: “This trial was particularly ambitious. This is the first time a study in progressive MS has evaluated the proportion of patients improved at M9 and confirmed at M12.”
MD1003 is an investigational medicine thought to have both pro-myelinotic effects and to enhance the supply of energy for nerve impulse transmission. MD1003 is an active pharmaceutical ingredient administered at a dose of 300 mg /day.
Source: Business Wire © 2015 Business Wire (07/04/15)
Patients could benefit from brain boost(07/04/15)
Multiple sclerosis patients could one day benefit from treatments that boost their brain function, a study has suggested.
Increasing the activity of neurons could be beneficial in people with the condition, researchers say. It could stimulate the production of a substance that protects nerve fibres.
The finding could pave the way for new treatments, researchers say. MS affects the brain and spinal cord and can cause problems with balance, movement and vision.
Information in the brain is transmitted along nerve fibres known as axons. A material - called myelin - forms a layer around axons, which keeps them healthy and helps speed up the transfer of information.
Damage to myelin contributes to diseases of the brain such as multiple sclerosis.
Until now, it was not known how brain activity controls production of myelin by specialist cells, researchers say.
Researchers examined how changes in the activity of neurons affects how much myelin is produced in the brains of zebrafish. Decreased brain function reduced the amount of myelin made, while production was increased by around 40 per cent when the neuronal activity of fish was increased, the team says.
Before they can develop new therapies, the team says it needs to learn more about how brain function controls the complex processes by which axons are coated with myelin.
The study, published in the journal Nature Neuroscience, was funded by The Wellcome Trust, the Biotechnology and Biological Sciences Research Council, and the Lister Research Prize.
Dr David Lyons, of the University of Edinburgh's Centre for Neuroregeneration, who led the study, said: "We have a long way to go before we fully understand how our brain activity regulates myelin production, but the fact that this is even something that the brain can do is a good news story. We are hopeful that one day in the future we may be able to translate this type of discovery to help treat disease and to maintain a healthy nervous system through life."
Source: Medical Xpress © Medical Xpress 2011-2015, Science X network (07/04/15)
A study published in PLOS ONE provides new insights into the relationship between the immune system and neurodegeneration and clinical disability in MS, reports Multiple Sclerosis News Today.
A team of researchers led by Dr. Shahin Aeinehband from the Neuroimmunology Unit at the Karolinska Institutet in Sweden looked at the association between a central component of the innate immune system, C3 protein, with the activity of cholinergic metabolism and neurodegeneration markers in both relapsing-remitting and primary progressive MS.
In the study Complement Component C3 And Butyrylcholinesterase Activity Are Associated With Neurodegeneration And Clinical Disability In Multiple Sclerosis, Dr. Shahin Aeinehband and his team analysed 48 samples of cerebrospinal fluid (CSF) from MS patients and compared them to 18 samples of CSF from healthy individuals. Levels of C3 protein; neurofilament-light (NFL), a marker for ongoing nerve injury; and activity of the two main acetylcholine degrading enzymes, acetylcholinesterase and butyrylcholinesterase (BuChE) were measured.
C3 protein levels were elevated in MS patients when compared to controls and were correlated both to disability and neurodegeneration (as showed by NFL levels). This finding supports the theory that the complement system influences MS and is compatible with previous findings in other neurodegenerative conditions. Additionally, the C3 protein levels were increased in patients with more cerebral lesions on magnetic resonance imaging and in patients with progressive disease. Finally, BuChE activity correlated with both C3 and NFL levels in individual samples.
In conclusion, the study found that C3 protein is a marker for ongoing nerve injury and degree of disease disability, with this relationship appearing to be especially important in late stage disease (i.e., with more cerebral lesions or clinically progressive disease). It also suggests a link between the expression of complement C3 and the cholinergic tone (BuChE activity).
Although further studies are needed to clearly establish the cause of these processes, these findings can offer future novel targets for MS therapy.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (07/04/15)
A group of researchers have been investigating the theory that high levels of uric acid, whch may have protective effects on neurons and are present in gout patients, could mean gout resulting in a reduced risk of developing neurological disease, reports Multiple Sclerosis News Today.
“This study investigated the epidemiological evidence for a protective role of high serum concentration of uric acid, for which we used gout as a proxy, in the aetiology of multiple sclerosis, Parkinson’s disease, or motor neuron disease,” wrote Dr. Pakpoor, who works alongside Dr. Michael J. Goldacre at the Unit of Health-Care Epidemiology in the University of Oxford. The article, “,” was published in the journal BMC Neurology.
Dr. Julia Pakpoor’s study, Clinical Associations Between Gout And Multiple Sclerosis, Parkinson’s Disease And Motor Neuron Disease: Record-linkage Studies, analysed patient records for hospital admissions and deaths in England between 1999 and 2012. Of approximately nine million hospital admissions, 214,653 were related to gout, 82,220 related to multiple sclerosis, 217,179 related to Parkinson’s disease, and 25,185 related to motor neuron disease.
When researchers analysed the long-term data from the study, patients with gout were not found to be less likely to develop multiple sclerosis. Although the odds ratios revealed a modest correlation between gout and subsequent multiple sclerosis, that observation was negated when the researchers only analysed neurological disease diagnosed within five years of a gout diagnosis.
On the other hand, patients with multiple sclerosis were less likely to experience gout, the study found.
Strengths of the study included a large sample size and a national representation of the population. However, since the study was not conducted in a cohort of patients, the researchers are limited in knowing if hospitalisations were “first ever” diagnoses. Additionally, gout is only a representation of increased serum uric acid, meaning the association between uric acid and neurological disease may be underestimated.
To remediate this limitation, the authors suggest the possibility of conducting a follow-up study of multiple sclerosis patients to identify the presence of gout or serum levels of uric acid over time.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (07/04/15)
Researchers at the IRCCS Centro Neurolesi “Bonino-Pulejo” and the University of Messina in Italy have performed a review on the immunomodulatory activity reported for statins in the treatment of multiple sclerosis (MS) and on clinical trial results, reports Multiple Sclerosis News Today.
The study, Role Of Statins In The Treatment Of Multiple Sclerosis, was published in the journal Pharmacological Research.
Statins have been shown to have immunomodulatory and anti-inflammatory properties, making them an attractive therapeutic option for immune-mediated disorders such as MS.
Previous studies conducted in vitro and in animal models showed evidence that statins also have potential neuroprotective properties, although the mechanism behind it is poorly understood. Based on these three properties— immunomodulatory, anti-inflammatory and neuroprotective — they have now been tested in clinical trials as a therapy for MS, either alone or in combination with interferon-beta. Unfortunately, the translation of the results obtained in animal models with statins yielded conflicting results in human clinical trials.
Researchers found some clinical trial studies indicated oral statins were only partially effective as a monotherapy in the treatment of relapsing-remitting MS. When tested in combination with interferon-beta, some studies found an increase in clinical disease activity, relapses and new lesions in the brain. Other studies, however, have reported the combination therapy of statin and interferon-beta had no effect on relapse rate, neither on the development of brain lesions in patients with relapsing-remitting MS. Yet, other studies found statins offer clinical benefits in comparison with interferon-beta treatment alone, namely in the number of relapses and lesions in MS patients.
The research team concluded that the therapeutic combination of statins plus interferon-beta is apparently well-tolerated and safe but could not find decisive proof that statins and interferon-beta improves relapsing remitting MS outcomes in comparison to treatment with interferon-beta only.
The research team suggests further large, prospective, randomized, double-blind, placebo-controlled trials should be conducted to assess and provide definitive proof of whether statins are effective, either as monotherapy or combined with interferon-beta, as a treatment for MS.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (02/04/15)
A new section has been added to healthtalk.org today to support family members and friends of people living with multiple sclerosis (MS).
The resource is based on the experiences of 40 people who shared their stories on film in interviews with University of Oxford researchers. Visitors to the website can find out what happens when a loved one has multiple sclerosis by reading about the experiences of others and watching clips from the interviews.
The new ‘MS: friends & family experiences’ section of healthtalk.org is comprised of 25 web pages and 250 video and audio clips and covers every aspect of life with multiple sclerosis from the point of view of friends and family, including topics such as social lives, relationships and feelings, as well as practical issues such as work, money, looking after home and family and home adaptations.
The research for the MS project was carried out by Nic Hughes, at the time a researcher from The Health Experiences Research Group (HERG) at the University of Oxford’s Nuffield Department of Primary care. Nic travelled around the country with a video camera, interviewing people in their own homes. Nic was supported in his research by a panel of expert including health professionals, researchers, interviewees from the project and a representative from the MS Society.
The group uses the same method for each health issue covered on healthtalk.org. Sara Ryan, Research Director for HERG explains “We use rigorous research methods to capture the full ranges of experiences a patient might expect, not just the more sensational stories or hearsay you might find online”. healthtalk.org (formerly healthtalkonline) is run by an online charity that provides information and support around health issues by sharing patient stories. “healthtalk.org was founded on the belief that patients can offer invaluable advice and wisdom to others that are going through the same thing.” says Jo Kidd, Communications Manager for the charity “People often tell us how relieved they feel to hear other people talk about their experiences, it reminds them that they aren’t alone.”
The new resource is available at: http://www.healthtalk.org/ms-friends-family
Soure: United Kingdom Multiple Sclerosis Specialist Nurse Association (UKMSSNA) (02/04/15)
Phase 1 trial completed(01/04/15)
Vaccinex, Inc. has today announced the successful completion of a multicenter phase 1, randomized, double-blind, placebo-controlled, single ascending-dose safety and tolerability study in adult patients with multiple sclerosis.
According to reports, a total of 50 patients took part in the trial to determine the safety and tolerability of the drug currently known as VX15/2503, a monoclonal antibody discovered, characterised, and successfully tested by Vaccinex in preclinical models of multiple sclerosis and Huntington's disease.
VX15/2503 was found to be well tolerated at dose levels of up to 20 mg/kg with no reports of treatment-related serious adverse events.
No maximum tolerated dose (MTD) was determined and no dose-limiting toxicities (DLTs) were observed.
A phase 2 clinical trial of the VX15/2503 antibody in Huntington's Disease is planned to begin in the first half of 2015.
Source: BioSpace Copyright © 2015 BioSpace.com (01/04/15)
The Austrian Centre of Industrial Biotechnology (Acib) claims to have developed a new purification method for pharmaceutical produced antibodies that promises to effectively decrease the high prices of these drugs in the market reports Multiple Sclerosis News Today.
For the pharmaceutical industry, decreasing processing costs is contingent on optimizing the purification process of antibody production. Currently, the process is performed through a process called “protein A” affinity chromatography (which purifies and concentrates antibodies out of a mixture into a buffering solution) and accounts for about 80 per cent of all the production costs.
The new purification method, developed by the Austrian Centre of Industrial Biotechnology (Acib) and the University of Natural Resources and Life Sciences Vienna (BOKU), consists of a tubular reactor where a Calcium-Phosphate flocculation is applied followed by precipitation of the purified proteins by cold ethanol. The reactor is built as a double-pipe heat exchanger that works in counter-current flow.
The newly developed method boasts a significantly higher performance when compared to the current “protein A” affinity chromatography in both purification speed and antibody yields. An additional advantage is that the current system apparatus is easily transferred to the new system.
The Austrian Centre of Industrial Biotechnology (acib) is an international network composed of several universities and pharmaceutical industries, including the Universities of Innsbruck and Graz, Graz University of Technology, the University of Natural Resources, Vienna and Joanneum Research and pharmaceuticals such as BASF, DSM, Sandoz, Boehringer Ingelheim, Jungbunzlauer, voestalpine, 3M or Clariant.
As an international Research Centre for Industrial Biotechnology, acib scientists are devoted to developing new methods that are more economic and eco-friendly, in order to substitute current technologies.
Prof. Alois Jungbauer, acib scientist, commented in a press release, “Our method shows great potential as a new platform technology for the pharmaceutical industry.”
For almost forty years, Monoclonal antibodies have formed the basis for several experimental multiple sclerosis therapies. Researchers have favored their use due to the fact that they function well as a targeted treatment for the disease. While antibodies are often used in more progressive cases of MS, due to the fact that they must be administered intravenously and can lead to infusion reactions, acib’s new process for creating therapeutic antibodies could at the very least help to further develop their application for a larger percentage of the patient population.
Source: Multiple Sclerosis News Today © BioNews Services 2015 (01/04/15)
This was initially a campaign set up to support people with ‘profound and multiple learning disabilities’ (PMLD) to gain access to public toilet’s appropriate to meet their needs. There are many people who need facilities that are ‘more than your standard wheelchair accessible toilet’, not just people with PMLD but those with CP, MS and other support needs.
A ‘Changing Places’ toilets facilities will include an overhead hoist (or mobile hoist if that is not possible), an adult size changing bench, room for two carers and a centrally placed toilet (amongst other fab equipment!).
The campaign has been very successful and there are now over 700 ‘Changing Places’ loos across the UK (with more planned!).
Their website states that there are 8,500 people with MS who would benefit from this level of accessibility.
The Changing Places website has an interactive map listing all the loos’ available and also a ‘postcode locator’.
It’s a great resource to promote and share.
Source: Changing Places (01/04/15)
MS drug 'may already be out there'(01/04/15)
Depression and heart-disease drugs are to be tested in a trial to find treatments for multiple sclerosis from existing medicines, reports the BBC.
There are currently no treatments in the secondary progressive stage of the condition and doctors hope the necessary drugs are already out there, but have never been tested on MS.
More than 400 people will take part in the trial at University College London and the University of Edinburgh.
Walking, balance, speech, and vision can all become impaired in the later stages of the disease.
There are treatments in the early phases of MS to prevent the frequency or severity of relapses but there is nothing once the symptoms progresses.
The MS-Smart trial will test the safety and effectiveness of three drugs used in other conditions:
Amiloride - licensed to treat heart disease
Fluoxetine - used in depression
Riluzole - for Motor Neurone Disease
They were identified after a review of previously published research into drugs that appear to protect the nerves from damage.
Researchers believe these treatments could slow down the progress of MS and the trial will be the first time they have been tested on such a large number of patients.
Dr Jeremy Chataway, a consultant neurologist and lead researcher on the trial based at UCL, said there was "huge unmet need".
He told the BBC: "It may be the case that we have already invented the drugs we need to treat MS.
"In the same way that aspirin was developed as a painkiller and is now used to treat stroke patients, we may well have invented the drugs that we need, we just don't know that they work in different situations than what they were invented for.
"One of the advantages is they are very cheap, and we know a great deal about them as they have been tested on millions of people around the world in their original indication.
"So it's much more of a running start when we use drugs that we aim to repurpose."
Prof Siddharthan Chandran, a clinical neurologist at the University of Edinburgh, said: "This is a landmark study that seeks to not only test three potential treatments, but also showcase a new approach to clinical trials for progressive neurological conditions."
MS-Smart is a phase two trial, making sure the drugs are safe and demonstrate sufficient effectiveness before they are tested in a larger number of people.
If successful, it could lead to new ways of using the existing drugs to modify the way the disease develops.
Source: BBC News © British Broadcasting Corporation 2015 (01/04/15)
People with chronic fatigue syndrome show a distinct pattern of immune system proteins in their spinal fluid, reports HealthDay - a finding that according to researchers could shed light on the "brain fog" that marks the condition.
The new study found that, compared with healthy people, those with chronic fatigue syndrome had lower levels of immune-system proteins called cytokines in the fluid that bathes the spinal cord and brain.
The exception was one particular cytokine, which was elevated in not only people with chronic fatigue, but also those with multiple sclerosis.
The finding could offer clues as to why people with chronic fatigue syndrome typically have problems with memory, concentration and thinking, said lead researcher Dr. Mady Hornig, a professor at Columbia University's Mailman School of Public Health in New York City.
The study also bolsters evidence that some type of immune dysfunction underlies the puzzling disorder, Hornig said.
Chronic fatigue syndrome is known medically as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. In the United States, it affects up to 2.5 million people, according to the Institute of Medicine.
In February, the IOM released a report affirming chronic fatigue syndrome is a legitimate medical condition that many health professionals still misunderstand or even dismiss as a figment of patients' imagination.
For the new study, reported March 31 in the journal Molecular Psychiatry, Hornig's team studied spinal-fluid samples from 32 people with chronic fatigue syndrome, 40 with multiple sclerosis, and 19 healthy people.
Overall, the researchers found reduced levels of most cytokines in chronic fatigue syndrome patients' spinal fluid, versus the two other groups. But one cytokine, eotaxin, was elevated in people with chronic fatigue syndrome and those with multiple sclerosis.
The significance of that finding is not clear yet, Hornig said. But she said eotaxin is involved in allergy-like immune responses.
There are some similarities between MS and chronic fatigue syndrome, Hornig added. MS patients suffer fatigue, and the disease is believed to be caused by an abnormal immune reaction -- in this case, against the body's own nerve tissue.
The precise cause of chronic fatigue syndrome is far from clear, but in general, it's thought to involve some type of immune system dysfunction, Hornig explained.
In a recent study, her team found that in people who've had chronic fatigue syndrome for a relatively short time - fewer than three years - cytokine levels in the blood were actually elevated. They dropped again, though, in people who'd had the disease for a longer time.
People in the current study had had chronic fatigue syndrome for about seven years. So the relatively low cytokine levels in their spinal fluid "parallel" what was seen in the earlier study, Hornig said.
"I think what we're seeing is an immune system exhaustion over time," Hornig speculated.
The theory is that the immune system may initially go into overdrive against an invader - like a virus - and then be unable to dial itself down, Hornig explained. That could account for the high cytokine levels in people who've had chronic fatigue syndrome for a short time.
Over time, though, the immune system may essentially wear itself down, leading to weak responses to mild infections that a healthy immune system would readily handle, Hornig suggested.
One hope, Hornig said, is that these findings could lead to objective tests that can diagnose chronic fatigue syndrome early.
Understanding the biology of the disease could also lead to treatments, Hornig said.
"We can't promise this will translate into treatments around the corner," she said. "But we hope to start giving doctors some tools."
Source: HealthDay Copyright ©2015 HealthDay (01/04/15)