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February 2010CCSVI or Blood Flow in the Brain and Venous Insufficiency in MS – Society Leaders Meet with Dr. Zamboni Today. Research Proposals Received from Around the World on February 9th Grant Request DeadlineSummary: Recent preliminary studies indicate that a phenomenon called CCSVI, a reported abnormality in blood drainage from the brain and spinal cord, may contribute to nervous system damage in MS. This hypothesis has been put forth by Dr. Paulo Zamboni from the University of Ferrara in Italy. Based on the results of his initial preliminary findings, Dr. Zamboni states that this pilot study warrants a subsequent larger and better controlled study to definitively evaluate the possible impact of CCSVI on the disease process in MS. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ January - 2010 $4.5 Million Appropriated to Continue Established MS Research ProgramWe are pleased to announce that $4.5 million has been appropriated within the FY 2010 Congressionally Directed Medical Research Programs (CDMRP) for multiple sclerosis research. This program is funded through the Defense Department at the direction of Congress and was signed today by the President. This latest appropriation is a continuation of the MS program that was founded in FY 2009. Other allies who helped petition Congress for this new MS research funding included the American Academy of Neurology, the Paralyzed Veterans of America, United Spinal, AMVETS, the Vietnam Veterans of America, and the Disabled American Veterans. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ 2009 A LOOK BACK ON WHERE WE HAVE COME SINCE LAST YEAR This year saw exciting research progress, with unprecedented opportunities on the horizon and more scientists than ever working on important questions. While the economic environment resulted in an unfortunate slowing of funding creating gaps in planned expenditures to support MS research, it is the hope this impact will be of short duration. Despite these challenges, the National MS Society continues to propel research forward and move us closer to a world free of MS. In 2009 the MS Society provided over $33.5 million to support 345 new and ongoing projects in it's research portfolio, plus $1.5 million for Fast Forward, the drug development subsidiary which continues to attract new funding streams. In addition, thanks to the efforts of MS activists, $5 million has been specifically set aside for funding MS research out of the 2009 Department of Defense budget. The MS Society has nimbly pursued promising opportunities when they arise, such as the recent request for research applications to expeditiously examine the potential impact of the chronic cerebrospinal venous insufficiency (CCSVI) hypothesis on disease process in MS. Here is just a small sample of the many important, potentially high-impact research results that occurred this year, which support the three research goals set out by our MS Society: stopping MS, reversing the damage and restoring function, and ending MS forever. STOPPING MS Several papers published this year provided more evidence that starting on MS therapies early after disease onset, or even before a definite diagnosis, can pay off later by delaying disease progression. In addition, results of clinical trials of oral therapies and therapies with infrequent dosing regimens were presented at medical meetings and in journal articles this year. So far, some appear to have benefit against MS attacks, and safety profiles look acceptable. Novartis International AG announced that ORAL FTY720 (fingolimod) significantly reduced relapse rates and slowed disability progression over two years on a large-scale, phase 3 trial in relapsing-remitting MS. According to the company, safety data confirmed a positive benefit-risk profile, and the company plans to seek marketing approval at the end of calendar year 2009. An oral drug was submitted to the FDA for marketing approval in September 2009. In a large-scale clinical trial, cladribine tablets significantly reduced relapse rates and other disease activity in people with relapsing-remitting MS. If the FDA application is successful, it would be the first approved oral disease-modifying therapy for MS. Positive results were announced by sponsors of a clinical trial of the experimental IV monoclonal antibody ocrelizumab, which significantly reduced disease activity on MRI scans in a study of 220 people with relapsing-remitting MS. Since this was a phase 2 study, additional research will be needed to further determine this drug's safety and benefits. An international task force convened by the MS Society published a landmark paper in the journal Multiple Sclerosis to guide neurologists through the complex process of distinguishing MS from look-alike disorders ("differential diagnosis"). This paper was the most frequently downloaded paper from the journal's Website this year. FAST FORWARD made its first investments in promising agents. This effort to speed the delivery of new treatments to people with MS has already attracted over $20 million in new funding. A small NIH-supported study by Stanford University researchers found that women who breast fed their babies exclusively (without giving supplemental bottles) for at least the first two months postpartum were less likely to have an MS relapse than those who did not breast feed or who did not breast feed exclusively during the first two months. Multiple previous studies have documented that smoking cigarettes increases the risk of developing MS. Harvard researchers have now tracked hundreds of smokers, ex-smokers and never-smokers, all of whom had MS, for an average of over three years. They reported that disability progressed more quickly in smokers. And in several measures, ex-smokers did not differ substantially from never-smokers, suggesting that quitting may delay MS progression. In two other separate studies, State University of New York, Buffalo researchers reported links between smoking and brain tissue damage observed on MRI scans of people with MS, and Karolinska Institute investigators in Sweden confirmed negative effects of smoking, but found no association between the use of Early, small-scale trials are underway or getting started to test the potential of a special type of adult stem cell found in the bone marrow, called mesenchymal stem cells. Although these cells have the potential for both turning down MS immune attacks and stimulating nervous system repair, it's still too early to know whether this approach will prove safe and beneficial. To help ensure that stem cell trials are conducted in a scientifically sound way that will move the field forward, the Society convened an international meeting with our counterparts in the U. K., Italy, and France to develop guidelines for stem cell trials, which are expected to be published in 2010. An international team funded in part by the National MS Society reversed MS in mice by administering lisinopril, a drug commonly used to lower blood pressure. A drug used to treat diabetes (metformin) also improved MS-like disease in mice in a study by Society-funded researchers from Medical University of South Carolina and Mayo Clinic. And researchers from Canada reported that mice recovered from MS-like disease when administered a compound called (GIFT15) formed by fusing two immune proteins. A European collective of imaging experts known as "MAGNIMS" published new information on imagine and clinical findings that might help explain why some people experience a mild course of MS, also known as "benign" MS. They recommended that cognitive functions, not just physical functions, be taken into account when labeling a person's MS as benign. The first large-scale clinical ("phase II") trial of the sex hormone estriol in MS, funded by the National MS Society and especially its Southern California chapter, along with the NIH, continued to recruit women with MS to participate, expanding the number of centers to 16 across the US. The two-year trial could lay the groundwork for a larger, definitive trial that could lead to a new treatment option for women with MS. REVERSING MS DAMAGE & RESTORING FUNCTION In response to reports that a phenomenon called CCSVI (chronic cerebrospinal venous insufficiency, a dysfunction of the brain blood flow and/or blood drainage) may contribute to nervous system damage in MS, the Society invited investigators to apply for grant funding and created an accelerated review process to explore this lead. If confirmed, this may open up new research avenues into the underlying pathology of MS and new approaches to therapy. The Society gathered together 70 members of the four international Promise: 2010 Nervous System Repair Teams to share progress and plan next steps to speed clinical trials of therapies to protect and reverse neurological damage. Each team reported impressive progress, with two of the teams about to launch new, small-scale clinical trials of different types of stem cells, with separate funding. Members of the Society's Nervous System Repair Team led by Professor Charles french-Constant (University of Edinburgh and University of Cambridge, UK) published a paper demonstrating that a complex network of proteins that interact during brain development (called the "Wnt signaling pathway") may also play an important role in the failure of nerve-protecting myelin to repair itself in people with MS. This could provide new clues to reversing myelin damage. After showing benefits for temporarily improving walking speed in all types of MS in two phase 3 clinical trials, an advisory committee for the FDA recommended marketing approval for Acorda Therapeutics' fampridine (with the proposed new name, Amaya). If approved, this oral drug would be the first approved specifically for managing MS symptoms. The National MS Society funded early stage studies in the development of this drug. Two groups funded by the Society reported findings on nerve tissue injury and repair that add important information needed to stop MS progression and develop nervous system repair strategies. Mayo researchers found two enzymes that may serve as markers of progressive MS and nerve fiber injury, and investigators at Mount Sinai School of Medicine (New York) reported that a different enzyme is essential for replenishing myelin-making cells that have been depleted by MS. An oral drug designed to treat uncontrollable laughing and/or crying (also called pseudobulbar affect), a troubling symptom experienced by some people with MS and other neurological disorders, passed another hurdle by showing positive results in a Phase 3 trial. According to company sources, Zenvia (Avanir Pharmaceuticals) significantly reduced the rate of laughing and crying episodes and appeared to be safe and well tolerated. ENDING MS FOREVER The Society launched a genetics study that should identify most of the common genes that contribute to making people susceptible to developing MS. In the short run this should set us up to discover new disease pathways that can be targeted for therapy. In the longer run, this should provide a map for preventing MS. Researchers at the University of Buffalo, New York and Italy reported two studies that add to growing findings linking the Epstein-Barr virus (EBV) with multiple sclerosis. One study suggested a link between EBV exposure and the loss of nerve tissue, while the other explored interactions between a person's genes and EBV. Two studies published in the journal Nature Genetics identified new genes and gene regions that contribute to making people susceptible to developing MS. The findings, by the International Multiple Sclerosis Genetics Consortium and the Australia/New Zealand MS Genetics Consortium, add to a growing list of gene variations linked to MS susceptibility. The National MS Society funded the formation of the International MS Genetics Consortium and studies by the Consortium. For the first time, researchers in the UK and Canada found evidence of a direct interaction between vitamin D and a common genetic variant, the presence of which increases the risk of developing MS. The research highlights the importance of studying the interaction of genes and the environment to search for the underlying triggers of this complex disease. The Society convened an international workshop focused on strategies to find the cause of MS, as well as factors that drive progression and ways to estimate MS frequency. One outcome from the workshop is the proposed funding of a two-year pilot project to plan a large study to determine risk factors that drive MS progression and predict prognosis. The Society also held the first-ever Don Tykeson Fellows Conference to stimulate new research ideas and strengthen the commitment of these bright young people to MS research. Supporting fellows, who are the future of MS research, is a key component of the Society's strategic plan. These and other leaps forward - accomplished in the midst of the worst economic downturn since the Great Depression - made 2009 a momentous year of progress toward a world free of MS. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ December - 2009 PANEL RECOMMENDS THAT FDA APPROVE FAMPRIDINE-SR (proposed name AMAYA) FOR SYMPTOMATIC TREATMENT OF MS -- FOUND TO IMPROVE WALKING SPEED FOR ALL TYPES OF MS A U.S. Food and Drug Administration advisory committee today recommended that the agency approve marketing of Fampridine-SR (Acorda Therapeutics, with a proposed name change to AMAYA) for its ability to improve walking speed in people with any type of multiple sclerosis. While the FDA is not required to follow the recommendations of its advisory committees, it usually does. The agency is expected to make a final decision about whether to approve the drug for market on or before the target date of October 22, 2009. During an all-day meeting held October 14, 2009, the FDA advisory committee considered Acorda Therapeutics' application for approval of Fampridine-SR, reviewing data about the drug's effectiveness and safety. The committee also heard public testimony from individuals and patient advocacy groups, including the National MS Society, which testified to the unmet need for therapies to improve walking for people with MS. Among its discussions, the advisory committee recommended that the FDA require the sponsor to evaluate the effects of doses lower than originally studied, but that these studies would not be required to be done prior to the drug's marketing approval. In addition, the FDA is likely to require a plan to mitigate potential risks. During its presentation to the committee, Acorda representatives outlined such a plan -- the Risk Evaluation Mitigation Strategies (REMS). BACKGROUND ON UNMET NEED: Problems with gait (difficulty in walking) are among the most common limitations in MS. While there are six FDA-approved disease-modifying therapies that are at least partially effective against some forms of the disease, as well as rehabilitation and symptomatic treatments for some symptoms, at present there is no pharmacologic treatment specifically available for MS-related difficulty walking. This disability has wide-ranging effects on people's lives, even in its milder manifestations. A recent survey among more than 1,000 individuals with MS and many of their family members examined the impact of mobility issues, such as difficulty walking, on quality of life among patients with MS and their families. Some two-thirds of patients reported difficulty walking and of these, 70% reported that such difficulty was the most challenging part of their MS, and most reported that difficultly walking restricts their daily activities significantly, including their ability to travel. ABOUT THE DRUG: Fampridine-SR is a sustained-release formula of 4-aminopyridine, which blocks tiny pores, or potassium channels, on the surface of nerve fibers. This blocking ability may improve the conduction of nerve signals in nerve fibers whose insulating myelin coating has been damaged by MS. The first studies of this potassium-blocking approach in people with MS were supported by the National MS Society. WHAT CLINICAL TRIALS FOUND: Acorda Therapeutics sponsored two phase 3 clinical trials of the drug. In the first, involving 301 people with any type of MS, walking speed increased by 25%. Results of this study have been published (February 28, 2009 issue of the Lancet (2009 373;732-738, summarized here). Results from a later, second phase 3 study involving 240 people with MS confirmed the benefits seen in the first, finding that a significantly greater proportion of people on the therapy had a consistent improvement in walking speed compared to those who took placebo. Among those taking Fampridine-SR who improved in walking speed, there was a statistically significant improvement in leg strength. In the first study, common adverse events (side effects) experienced more often by those on active treatment included back pain, dizziness, insomnia, fatigue, nausea and balance disorder. Two serious adverse events led participants to discontinue taking the drug (one case of anxiety and one seizure in a person who developed sepsis from a urinary tract infection). In the second study, additional common adverse events in those on therapy included urinary tract infection, falls, and headache. Further study and clinical practice may help determine the extent to which the drug may impact other functions not measured in the clinical trials, and provide hints as to which patients are most likely to respond. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ WALKING (GAIT), BALANCE, & COORDINATION PROBLEMS Problems with gait (difficulty in walking) are among the most common mobility limitations in MS. Gait problems are related to several factors.
Most gait problems can be helped to some extent by physical therapy (including exercises and gait training), the use of appropriate assisting devices and, in some cases, medications. Careful evaluation by a trained health care professional is essential for creating the appropriate therapy program for each individual. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ November - 2009 POSITIVE RESULTS PUBLISHED OF FIRST OF TWO PHASE 3 CLINICAL TRIALS OF FAMPRIDINE-SR Walking speed improved significantly in a phase 3 clinical trial of 301 people with all types of MS taking oral Fampridine-SR (Acorda Therapeutics, Inc.), a drug designed to provide symptomatic relief by compensating for lost nerve conduction. Fampridine-SR is a sustained-release formula of 4-aminopyridine, which temporarily enhances nerve signaling by blocking tiny pores, or potassium channels, on the surface of nerve fibers. A paper describing the study, by Dr. Andrew Goodman (University of Rochester) and colleagues, is published in the February 28, 2009 issue of The Lancet (2009 373;732-738). Results from a later, second Phase 3 study, announced in 2008, confirmed Fampridine's benefits reported here. In early February 2009, Acorda announced that it had applied to the FDA for marketing approval of Fampridine for multiple sclerosis. BACKGROUND: Problems with gait (difficulty in walking) are among the most common mobility limitations experienced by people with MS. Fampridine-SR is a sustained-release formula of 4-aminopyridine, which blocks tiny pores, or potassium channels, on the surface of nerve fibers. This blocking ability may improve the conduction of nerve signals in nerve fibers whose insulating myelin coating has been damaged by MS. The first studies of this potassium-blocking approach in people with MS were supported by the National MS Society. THE STUDY: A total of 301 people with all types of MS participated at 33 sites in the U.S. and Canada. Participants were randomly divided such that 224 were on active treatment and 72 were on inactive placebo over 14 weeks. Participants were permitted to remain on other medications during the trial, establishing the potential of the drug as a symptomatic management strategy that could be used along with their regular medications and disease-modifying therapies. RESULTS: Thirty-five percent of those on active therapy, versus only eight percent of the placebo group, experienced significant improvements in walking speed. The walking speed for those who responded to therapy improved an average of 25.2% (in the timed 25-foot walk), compared to only 4.7% in the placebo group, and the improvement was maintained over the 14 weeks of therapy. Improvement was also noted in the "MS Walking Scale 12", a measure designed to assess how meaningful the improvement was for individuals; in this study, those who responded to the drug reported feeling less disabled in daily activities requiring mobility. Other positive outcomes included increased leg strength in those on active treatment, even in some individuals whose walking speed did not improve. Common adverse events (side effects) experienced more often by those on active treatment included back pain, dizziness, insomnia, fatigue, nausea and balance disorder. Serious adverse events that led to discontinuation of the drug included one case of anxiety and one seizure in a person who developed sepsis from a urinary tract infection. There were no deaths during the treatment phase of the study, but one person died five weeks after the last treatment visit of heart disease, which was deemed by investigators to be unrelated to the therapy. Results from a later, second phase 3 study, announced in 2008, confirmed the benefits seen in this trial. The company announced that it had applied to the FDA for marketing approval of Fampridine in early February 2009. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ October - 2009 FLU VACCINE AND H1N1 (SWINE FLU) VACCINE INFORMATION FOR 2009-2010 REGULAR FLU SHOT: As in previous years, the National MS Society recommends a regular flu shot as a safe and effective vaccination for people with MS. The flu shot - which is a de-activated or "killed" vaccine - can safely be taken by individuals who are on any of the disease-modifying medications (Avonex, Betaseron, Copaxone, Rebif, Novantrone, or Tysabri), (all are registered trademarks of their respective companies). FluMist INTRANASAL: In 2003, the FDA approved a flu vaccine nasal spray "for healthy children and adolescents, ages 5-17, and healthy adults, ages 18-49." According to Dr. Aaron Miller, the Society's Chief Medical Officer, FluMist--which is a live, weakened vaccine--is not recommended for use by people with MS, and should specifically be avoided by any person with MS who is on an immunosuppressive medication such as mitoxantrone (Novantrone), cyclophosphamide (Cytoxan), azathioprine (Imuran), or methotrexate, (all are registered trademarks of their respective companies).
H1N1 (SWINE FLU) VACCINE: The H1N1 (Swine Flu) vaccine is still in production, so its safety and efficiency have not yet been established. It is anticipated that the vaccine will be available in the fall of 2009, probably in October. When it becomes available, the recommendations for its use in people with MS will likely be the same as the recommendations for the regular flu vaccine. If a live, attenuated version of the H1N1 vaccine is also produced, it should be avoided by individuals with MS. The initial supply of H1N1 vaccine will not be adequate to vaccinate everyone. The CDC has indicated that five groups will initially be targeted for vaccination:
It is important to note that people with disabilities (including people with MS) are not necessarily considered part of this high-priority group. However:
We recommend that people talk with their MS doctor to determine if they are a good candidate for the H1N1 vaccine. IN SUMMARY:
____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ September - 2009 BREASTFEEDING MAY REDUCE LIKELIHOOD OF POSTPARTUM MS ATTACKS Annette Langer-Gould, MD, PhD (Stanford University) and colleagues followed 32 pregnant women with MS, assessing their disease and breastfeeding status at intervals out to 12 months after giving birth. They found that women who breast fed their babies exclusively (without giving supplemental bottles) for at least the first two months postpartum were less likely to have an MS relapse than those who did not breast feed or who did not breast feed exclusively during the first two months (36% who breast fed exclusively experienced a relapse, as compared to 87% who did not breast feed or who supplemented with formula). This pilot study, funded largely by the National Institutes of Health, was presented at the 2009 American Academy of Neurology meeting and was published early online in the Archives of Neurology on June 8th, 2009. While the study is small, it focuses attention on a quandary facing women with MS and their doctors: the crucial time period after giving birth, when there is a higher risk for relapse, and many women are advised to go back on their disease-modifying therapies as soon as possible. Since there is insufficient evidence to support the safety of breastfeeding while using any of these therapies, most babies born to moms with MS are bottle fed, despite known health benefits of breastfeeding for infants. More research is needed to help guide postpartum treatment decisions. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ August - 2009 TWO STUDIES FIND NEW GENES & GENE REGIONS THAT MAKE PEOPLE SUSCEPTIBLE TO MS Two studies recently published in the journal Mature Genetics report identifying new genes and gene regions that contribute to making people susceptible to developing MS. The findings, by the International Multiple Sclerosis Genetics Consortium and the Australia/New Zealand MS Genetics Consortium, add to a growing list of gene variations linked to MS susceptibility. Identifying all MS genes will likely lead to the development of more effective ways to treat the disease, and open the door to uncovering the cause of MS, which may lead to its prevention. In an analysis of several genome-wide scans, Philip De Jager, MD, PhD (Brigham & Women's Hospital, Boston) and colleagues in the International Multiple Sclerosis Genetics Consortium (IMSGC, a group of international MS genetic experts created with funding from the National MS Society) report that three genetic variations appear to make people more susceptible to developing MS, including genes that instruct the immune messenger proteins interferon beta and tumor necrosis factor-alpha. (Nature Genetics, Published online: June 14th, 2009) This adds to earlier work by the Consortium and other independent investigators, who have now identified scores of genes that may contribute to MS susceptibility. A small number of these have already been validated and many are currently undergoing validation (confirmatory) studies. Justin Rubio, PhD (Florey Neuroscience Institute, Melbourne) and colleagues in the Australia and New Zealand Multiple Sclerosis Genetics Consortium (ANZgene, supported by MS Research Australia, among others) published the results of a large-scale gene scan that confirmed the association of several genetic variations previously reported to be linked to MS, and identified two loci (regions on the chromosome where genes are located) on Chromosomes 12 and 20 that have been linked to other autoimmune disorders, but not yet to MS. (Nature Genetics, Published online: June 14th, 2009) A major effort has been under way for over a decade to search for the genetic underpinnings of MS - the inherited set of genes that make people susceptible to the unknown triggering factor or factors that lead to the disease. If successful, it would give scientists a roadmap to the cause of MS, as well as to concrete targets for new therapies and possibly even ways to prevent the disease. This painstaking search, involving analysis of the genome (all the genes within the body) and the banking of thousands of DNA samples from patients and family members, was jump started when the IMSGC used cutting-edge gene-chip technology to complete the largest replicated whole genome scan for MS yet in 2007. Now, only two years later, the IMSGC and other groups are taking full advantage of these technologies to identify more and more genes that seem to predispose people to MS. This international group pooled together data from three separate genome-wide studies in people with MS, including 895 people with MS genotyped in its original scan. Genetic material from a total of 2,624 people with MS and 7,220 controls without MS were analyzed, and replicated in a sample of 2,215 people with MS and 2,116 controls without MS. The study confirms that three new genetic variations are associated with MS; these variations exist in the genes for interferon regulatory factor 8, tumor necrosis factor receptor super family member 1A, and CD6 - immune messenger proteins. The data may indicate that these proteins are involved early on in the development of MS, note the authors. With support from the Wellcome Trust, the National MS Society and other sponsors, the IMSGC is conducting a very large scale genetics project to validate their discoveries and identify all remaining genes that exert significant effects on MS susceptibility. An Australian group compared genetic material from 3,874 people with MS and 5,723 people without MS in search of gene variations that appeared to make people more susceptible to developing the disease. They confirmed several gene variations that had been identified in previous studies, including the immune system-related genes CD58, HLA-DR15, IL2RA, and IL7R. The team also identified two loci on Chromosomes 12 and 20 that have been associated with other autoimmune diseases such as rheumatoid arthritis, but not yet with MS. Further study is necessary to determine the exact nature of the genetic variations at work in MS within these loci, but the authors note one interesting candidate -- CYP27B1 on chromosome 12, a gene that instructs vitamin D. There is growing evidence that vitamin D may help protect against the development of MS. "The pace of advancing genetics technology must by matched by the willingness of researchers to work together worldwide, and of people with MS to participate in genetics research," says John Richert, MD, Executive Vice President of Research & Clinical Programs at the Society. "These studies demonstrate the highest degree of collaboration among people dedicated to a world free of MS. We are fortunate to be witnessing this exciting era in MS genetics." ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ July - 2009 WHY DO SOME PEOPLE HAVE A MILD COURSE OF MS? MRI experts weigh factors that may help determine when MS is "Benign". "MS is notoriously unpredictable in its course," commented John R. Richert, MD, a neurologist and head of the Society's research and clinical programs, "and there's no way to reliably predict over the long run whether a person will experience a mild or severe course." Finding a way to predict who will have a mild course of MS would allow doctors to give better advice, and possibly spare some individuals from the expense and inconvenience of taking an MS therapy. "Right now, the best advice we can give is to get on an MS therapy as soon as possible following a definite diagnosis of MS with active disease, and for many even after experiencing a first attack that puts them at high risk for developing MS," said Dr. Richert. That's because at the time of diagnosis and for years thereafter, it is impossible to know if the disease will be benign or more active, and early treatment is the best defense we have for slowing this disease. Beyond prognosis, studying benign MS also holds promise for people with all types of MS: If we knew what made some people experience a mild course, that knowledge might be translated into slowing down the disease in people who experience more active MS. A collaborating group of imaging experts from Europe, called MAGNIMS, recently held a workshop to review major MRI (magnetic resonance imaging) studies that have been done in people who had a benign course of MS (mild MS over 15 or more years), in comparison to those with more typical courses. MRI offers a window to MS activity in the brain that often doesn't show up as obvious symptoms. The workshop results were recently published in the journal Neurology. The investigators were seeking flags that might distinguish people with mild MS from those with more disabling forms of the disease, and also clues to what factors make a person's MS course mild. While there was no slam-dunk -- no clear-cut MRI findings that were consistently unique to people with a benign course - they uncovered some significant trends. In general, compared to more active forms of MS, they found that people with a benign course had fewer areas of damage (lesions) and shrinkage (atrophy) in specific areas of the brain critical to movement and other important functions that contribute to disability. These factors, along with the ability of the brain to compensate for damage by moving functions to other regions of the brain (a phenomenon called brain plasticity), may account for the milder course in people with benign MS. Further research is needed to understand benign MS and to find early predictors that would help doctors advise people in their care. "The group's urging that neurologists take into account individuals' cognitive functions, not just their physical functions, when labeling a person's MS as benign is an important one, and should lead to a refined definition of benign disease," commented Dr. Richert. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ June - 2009 TEAMS FUNDED BY THE MS SOCIETY REPORT ON KEY ENZYMES RELATED TO MS PROGRESSION AND NERVOUS SYSTEM REPAIR Two teams of researchers funded by the MS Society have reported findings on nerve tissue injury and repair that add important information needed to stop MS progression and develop nervous system repair strategies. Isobel Scarlsbrick, PhD (Mayo Clinic and Foundation, Rochester, MN) and colleagues have found two enzymes that may serve as markers of progressive MS and nerve fiber injury. Patrizia Casaccia, MD, PhD (Mount Sinai School of Medicine, New York) and colleagues reported that another enzyme is essential for replenishing myelin-making cells that have been depleted by MS. Both teams are continuing these lines of research in hopes of identifying targets for the development of new therapies for MS. Dr. Scarlsbrick reported her team's findings related to MS progression at the annual meeting of the American Neurological Association (Abstract T-99). Dr. Casaccia's report on the enzyme critical for repair appeared in Nature Neuroscience. PROGRESSIVE MS AND KLK ENZYMES (DR. SCARISBRICK'S TEAM): Understanding the processes that lead to tissue damage in MS is crucial to feed parallel efforts to protect and repair the brain and spinal cord. Dr. Scarisbrick previously found elevated levels of "KLK6" (a newly identified member of the kallikrein enzyme family) in areas of damage found in tissue samples from people with MS. Now, in a follow-up study, the group has studied the levels of KLK6 and other kallikreins in blood samples taken from 35 people with different clinical courses of MS and 62 controls without MS. The results show that KLK1 and KLK6 were elevated in people with MS, with the highest levels appearing in people with secondary-progressive MS (a course of MS that initially is relapsing-remitting and then becomes progressive, with or without occasional relapses and minor remissions). The team also exposed nerve cells isolated from mice to KLK1 or KLK6 in the laboratory, and found that the enzymes promoted nerve cell loss. Dr. Scarisbrick is continuing to study the role of these enzymes in nerve fiber injury and hopes to find a way to target them with therapeutic strategies for people with progressive MS. REPAIR AND HDAC ENZYMES (DR. CASACCIA'S TEAM): MS involves immune attacks against brain and spinal cord tissues, primarily myelin, the insulation that surrounds and protects nerve fibers. Several studies have indicated that, early in the disease, immature myelin-making cells - called, "oligodendrocyte progenitors" - are recruited to generate new myelin. A sufficient number of these cells is needed so that progenitors can migrate to the site of myelin damage and develop into myelin-making cells. Then, genes that instruct the formation of myelin components are activated and myelin is formed. In MS, this process fails. Dr. Casaccia is studying whether some molecules may inhibit the activation of the genes that promote myelin formation. In this study, Dr. Casaccia's team observed the gene activity during oligodendrocyte development in mice with damaged myelin. They found that enzymes called histone deacetylases (HDACs) were crucial to this process, particularly HDAC1 and HDAC2. Deleting these two enzymes impaired the differentiation of oligodendrocyte progenitors, that is, the process by which these cells develop a more specialized form or function. The team is studying how these findings might be translated into therapeutic strategies. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ May - 2009 REPAIRING DAMAGED TISSUES Decades of research into nerve physiology, MS tissue damage and the biology of glial cells - the numerous brain cells that support nerve cells - have been laying the groundwork for finding ways to restore normal function in individuals with MS. Nervous System Repair and Protection teams funded by the MS Society's Promise: 2010 initiative are taking this research to the next level, with a goal of placing nerve tissue-protective treatments in clinical trials by the year 2010. Other research on this topic focuses on the micro-environment of the brain and conditions conducive to stimulating natural repair, and the potential for cell therapies. Exploring glia, which include cells in the nervous system that make nerve-insulating myelin, is a cornerstone of MS research. Myelin appears to be the main target of the immune attack in MS. The cells that make myelin - oligodendrocytes - also are lost in MS. Researchers study aspects of myelin that make it an immune target, and ways that some brain cells can contribute to the immune attack. They are also looking at factors that are important to the growth and development of oligodendrocytes and myelin, to find ways of promoting myelin repair. The aim of repairing the nervous system is to achieve an actual reversal of the damage caused by MS and to restore function. When myelin is damaged or destroyed, electrical conduction along the nerve fiber is impaired or stopped. Decades of research on myelin and myelin-making cells make it clear that natural myelin repair occurs, and key molecules and growth factors are being identified that may serve as targets for stimulating myelin repair. In recognition that during the course of MS the nerve fibers, or axons, are also damaged, a new research focus has emerged: in order to repair the nervous system, we must learn how to regenerate axons as well as myelin. Insights into complex mechanisms involved in nervous system development now make it feasible to aggressively address the task of repairing axons as well as myelin in MS. Approaches to repairing the nervous system are varied. Some are aimed at inducing the body's own cells to more adequately carry out the repair function. Another approach is to introduce replacement cells from a different source. Research into the potential of stem cell therapy is proceeding rapidly, using cells obtained from a variety of adult and non-adult sources. It is currently not clear which source of stem cells, if any, will be of value in treating people with MS. Similarly, if more than one source proves to be valuable, it is not clear which will be best. The MS Society and the MS International Federation sponsored a Stem Cell Summit meeting in January 2007 to begin to determine how best to answer these questions. This is a field that is in its earliest stages of development, and the Society is funding research studies that will lead to significant advances in our knowledge on this front. In conjunction with the efforts to repair axons are new efforts to protect them from degeneration in the first place. For example, it is not clear whether axonal degeneration in MS results from a direct attach on axons by the immune system or, alternatively, if the loss of myelin by itself is enough to cause axonal degeneration (i.e., whether myelin has a protective effect on axons that is lost in the MS disease process). The protection of axons from these and other insults are a new area of intense research efforts in MS. The Nervous System Repair and Protection Initiative, funded through Promise: 2010 is bringing the dream of protecting and repairing brain tissue and restoring function within our grasp. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ April - 2009 EPIDEMIOLOGIC STUDIES HAVE GIVEN US SOME IMPORTANT CLUES ABOUT WHO DEVELOPS MS
Epidemiological studies ultimately seek to discover the cause of MS, and may also serve as the basis for developing future treatments. Many investigators believe that no single infectious agent or environmental factor is "the" cause of MS. Rather, they are exploring how a susceptible person's immune system reacts to a variety of viral or other infections and environmental exposures, and how immune function is linked to hormonal and other factors. The National MS Society is currently funding several research projects related to MS epidemiology and infectious triggers. These include:
____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ March - 2009 NATIONAL MULTIPLE SCLEROSIS SOCIETY AND ALL THOSE BATTLING THIS DISEASE COMMEND PRESIDENT OBAMA'S STEPS IN REMOVING THE BANS ON EMBRYONIC STEM CELL RESEARCH The National Multiple Sclerosis Society is a driving force in creating a world free of MS. To advance this goal, the Society continues to seek ways to prevent, slow the progression or repair the effects of MS. One channel is by supporting scientifically meritorious medical research, including research using human cells. This is done in accordance with federal, state and local laws and with adherence to the strictest ethical and procedural guidelines. For the past eight years, federal policies have impeded these efforts by severely limiting the number of approved embryonic stem cell lines that could be used in federally funded research and prohibiting the donation of unused embryos for research purposes by people utilizing the services of in vitro fertilization clinics. President Obama has taken a major step in removing the barriers to a promising path of responsible scientific research and the Society commends him for the new hope and optimism he brings to the millions of people living with chronic and debilitating diseases or disabilities. GENETICS STUDIES YIELD NEW CLUES TO WHY PEOPLE GET MS New studies are deciphering the complex picture of genetic characteristics that make people susceptible to MS. Each gives important new clues about why people get MS. Additional large-scale studies, the first stages of which are already underway, promise to uncover the great majority of genes that convey risk for MS, which would pave the way for understanding the basic cause of MS and developing more rational therapies. CD58 Gene: When it completed the largest replicated whole genome scan (scan of all the genes in the body) for MS to date, the International MS Genetics Consortium (IMSGC) identified and validated variations in two genes that help regulate the immune system as clearly increasing genetic susceptibility to MS, and preliminarily identified several other genes of newly suspected importance in MS. Philip De Jager, MD, PhD (Brigham & Women's Hospital, Boston) and colleagues in the IMSGC now report on one of these other genes, CD58, which instructs the activation of T cells, major players in the immune attack on the brain and spinal cord in MS. They studied this gene in 1530 additional people with MS, and found further evidence of its association with the disease. They pinpointed a specific marker, or segment of DNA, on the gene that is associated with reduced susceptibility to MS. They also showed that the level of CD58 expression (that is, the amount of CD58 protein that is produced from the CD58 gene) is associated with remissions from MS disease activity. Manipulating CD58 is a strategy used to treat other autoimmune diseases, so this study may open up new therapeutic options for people with MS. KIF1B Gene: Yuri Aulchenko, PhD, Rogier Hintzen, MD, PhD (Erasmus MC University Medical Center, Rotterdam, Netherlands) and colleagues completed a genome-wide study of a unique group - 26 people with MS in the Netherlands who had a common ancestor - a fact unknown to them before the study! They found evidence of heightened risk of developing MS associated with a variant of the gene KIF1B, which is important in the function of nerve cells. The team then sought to confirm these finding in a sample of 2,634 people from the Netherlands, Sweden, and the Canadian Collaborative Project on Genetic Susceptibility to MS, and a group of 2.930 controls without MS. The results strengthened the conclusion that the KIF1B variant is associated with significantly higher risk for developing MS. Since this gene is related to nerve cell function, it may also eventually help to determine why people with MS develop the long-term disability that results from nerve cell damage. HLA Gene: Stacy J. Caillier, BSc, Jorge Oksenberg, PhD (University of California, San Fransisco) and colleagues have been collecting blood samples from a large number of families affected by MS, funded in part by the National MS Society, focusing on ethnic groups with lower MS susceptibility (e.g., African-Americans) and higher susceptibility (e.g., individuals of Northern European descent), and searching for commonalities and differences that may help pinpoint genes of importance in MS. Here they report an important new finding on HLA genes, which are involved in immune function and have long been associated with MS. The team tackled the problem of how to discern the roles of two different closely related HLA genes - HLA-DRB1 and HLA-DRB5 - by studying a data set of 1635 African-Americans, including 769 people with MS. They found that HLA-DRB1 is associated with MS susceptibility even in the absence of HLA-DRB5, indicating that the former is the primary gene relating to susceptibility. People without HLA-DRB5 were at increased risk of developing secondary-progressive MS, however, this gene may protect against disease progression. GPC5 Gene: This same team completed a genome-wide study of genetic variations in 978 people with MS and 883 controls without MS. One of their most compelling findings is a link between the GPC5 gene with MS risk. This gene is implicated in nerve fiber regeneration, and previous work by this team suggested that variations in the gene may also help determine a person's response to interferon beta therapy. The team also found that genes relating to MS susceptibility were separate from those linked to disease course. "Each of these studies give us important new clues to why people get MS and even why it may progress," said John Richert, MD, Executive Vice President of Research and Clinical Programs for the National MS Society. "Of the genes identified so far, some function within the immune system and some are related to nervous system function. There is increased excitement and opportunity to study the many genes related to susceptibility and severity of MS", he added. "In fact, we're currently raising funds for a new international, large-scale study, the first stages of which are underway, that promises to uncover most of the remaining genes that convey risk for MS. This would pave the way for understanding its root causes and for developing more rational therapies and even prevention." ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ February - 2009 INTRIGUING LEADS ON THE HORIZON Decades of basic and applied research into MS and the basic workings of the immune and nervous systems have built a critical platform of knowledge that is serving as a springboard for progress. At the same time, new technologies, such as gene chip technology and new MRI-based imaging techniques, are allowing scientists to revisit age-old questions about MS, and may lead to insights into what causes this disease and what can be done to stop it and reverse its damage. Researchers are tracking down exciting leads and making headway in virtually every field related to MS. Here are some examples: **** THE FARTHER ONE LIVES FROM THE EQUATOR, THE HIGHER ONE'S RISK OF MS. Society researchers are exploring whether sunlight exposure is a protective factor, and are looking at many other risk or protective factors for clues to the cause of MS. **** CAN ROBOTICS RETRAIN THE BRAIN TO IMPROVE WALKING ABILITY? Based on the idea that repetition can help restore strength, balance, and recognition of sensory cues that make walking possible, improving walking ability. **** MS IS UNPREDICTABLE. Any individual's disease progression, severity, specific symptoms and response to therapies cannot be easily foreseen. But an international team of researchers is taking clues from patterns of MS damage seen in the brain to try to predict the best treatment for any individual. **** WOMEN ARE MORE PRONE TO DEVELOPING MS, but when men get the disease, it can be more severe. **** OUR BRAINS HAVE STORES OF CELLS CAPABLE OF REPLACING MYELIN. Can scientists find a way to stimulate these cells to repair MS damage, or do cell transplants hold more promise? Society researchers are on the cutting edge of these important questions. **** RESEARCHERS BELIEVE THAT A PERSON'S GENES DETERMINE WHETHER THEY ARE SUSCEPTIBLE TO DEVELOPING MS, yet even identical twins have different risks for the disease, depending on their experiences. **** MS COSTS THE U.S. ECONOMY ABOUT $28 BILLION PER YEAR. Our health care delivery and policy researchers are investigating this and other important issues, such as job discrimination, insurance experiences, and optimal health care settings. **** DEEPER UNDERSTANDING OF DESTRUCTIVE AND PROTECTIVE IMMUNE FACTORS IN MS, is opening up new opportunities for turning off the attack or to protect brain tissues. Experimental therapies in the pipeline include some in pill form. YEH! ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ January - 2009 TREATING MS SYMPTOMS WITH STEM CELLS Dr. Richard Burt and colleagues at Northwestern University report on the safety and benefits from an early phase study of experimental transplantation of individuals' own blood stem cells to turn off the immune attacks in MS. Unlike some of the previous studies of this procedure, this one involved 21 people with relapsing-remitting disease, rather than people with later stage, progressive disease. (The study results were reported early online on January 30, 2009 in Lancet Neurology.) In this uncontrolled trial, they found that the procedure was relatively safe, and after an average of 37 months, none had progressed and a significant portion experienced a reversal of at least 1 point on their disability (EDSS) scores, and 76% remained free from relapses. As pointed out by the investigators, it will take larger-scale, controlled trials to determine whether this expensive, potentially risky procedure is superior to other approved treatment options. Controlled trials of this procedure are now recruiting participants. Autologous hematopoietic stem cell transplantation is similar to bone marrow transplantation to treat cancer, except that it uses the patients' own blood or bone marrow stem cells. In treating MS, the procedure generally involves removing, from the blood stream, a person's cells that are capable of regenerating into new immune cells. These "stem cells" are stored, and the rest of his or her immune cells are destroyed by various chemotherapy or other regimens. Then the stored stem cells are reintroduced by injection. Eventually they grow and repopulate the body with immune cells. The hope is that the new immune cells will no longer attack myelin or other brain tissue, so that the person has perhaps a completely new immune system. However not with out risk. This procedure is strictly investigational, and it carries the risk of death because the body is nearly helpless against infection during the several weeks it takes for the immune system to be restored. There is no proof yet that it can cure a person with MS. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ December - 2008 YOUNG RESEARCHERS SHINE The MS - Society's 2008 National Conference brought together nearly a hundred young research fellows to add their voices and talents to solving the puzzle of MS. History shows that scientific breakthroughs often come from new thinking, fresh ideas, and young people. The conference is encouraging young scientists ready to embark on careers in biomedical research to focus on the final path of finding the way to stop MS in it's tracks. The conference aimed to promote the sharing of research information among research fellows and faculty grant recipients, develop a sense of community among investigators, stimulate new research ideas, and strengthen commitment to MS research. "I'm new to the field of MS, and I'm gratified to see how collaborative everyone is," said Daniel C. Tanner, PhD, a fellow at the University of Rochester. Twenty-one fellows presented their work on strategies to stop immune attacks against myelin and other central nervous system tissues in MS, including: >< Yueting Zhang, PhD (Mount Sinai School of Medicine) presented findings from a team led by her mentor Gareth John, VetMB, PhD, on immune messenger protein interleukin-11. The team found that this protein promotes the survival and maturation of myelin-making cells, leading to increases in myelin formation in tissue samples from people with MS. >< Philip L. Jager, MD, PhD (Brignam & Women's Hospital) reported on his team's finding that CD58, a possible location for one of many MS susceptibility genes, appears to contain genetic variations relevant to inflammation as well as nerve degeneration, but that these may be genetically distinct processes. >< Ellen Mowry, MD (University of California, San Francisco), a Sylvia Lawry Physician Fellow training to conduct MS clinical trials, presented her team's findings that someone whose initial MS event is resolving the unpredictability of MS. "You can read about MS in medical papers," said fellow Jennifer, PhD, of Harvard University. "But what you learn from talking to someone with the disease is so much more real." Dr. Kanter, whose father had MS, encouraged her colleagues to participate in Walk MS and Bike MS. She participates in the 50-mile Challenge Walk with her mother and sister. "If you want to feel the happiness that you get when an experiment goes well, go to a National MS Society event -- you'll feel it every time!" she said. A second Fellows Conference is planned for 2010, "It was great to meet so many people who have a common passion," said Astrid Cardona, PhD a Career Transition Fellow at the Cleveland Clinic Foundation. "How could we fail with all those great people behind us!" ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ November - 2008 LEUKEMIA DRUG CAN HALT, REVERSE MS LONDON (AFP) - Researchers at the University of Cambridge said Thursday they have found that a drug originally developed to treat leukemia can halt and even reverse the debilitating effects of Multiple Sclerosis (MS). In trials, alemtuzumab reduced the number of attacks in sufferers and also helped them recover lost functions, apparently allowing damaged brain tissue to repair so that individuals were less disabled than at the start of the study. "The ability of an MS drug to promote brain repair is unprecedented," said Dr. Alasdair Coles, a lecturer at Cambridge University's department of clinical neuroscience's, who coordinated many aspects of the study. "We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue." The MS Society, Britain's largest support charity for those affected by the condition, said it was "delighted" at the trial's results, which must be followed up with more research before the drug can be licensed. "This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in and day out," said head of research Lee Dunster. MS is an auto-immune disease that affects millions of people worldwide, including almost 100,000 in Britain and 400,000 in the United States. It is caused by the body's immune system attacking nerve fibres in the central nervous system, and can lead to loss of sight and mobility, depression, fatigue and cognitive problems. There is NO cure, and few effective treatments. In the trial, 334 patients diagnosed with early-stage relapsing-remitting MS who had not previously been treated were given alemtuzumab or interferon beta-1a, one of the most effective licensed therapies for similar MS cases. After three years, alemtuzumab was found to reduce the number of attacks the patients suffered by 74% over the other treatment, and reduce the risk of sustained accumulation of disability by 71% over interferon beta-1a. Many individuals who took alemtuzumab also recovered some of their lost functions, becoming less disabled by the end, while the disabilities of the other patients worsened, the study in the New England Journal of Medicine said. Alastair Compston, professor of neurology and head of the clinical neuroscience's department at Cambridge, said alemtuzumab was the "most promising" experimental drug for the treatment of MS. He expressed hope that further trials "will confirm that it can both stabilize and allow some recovery of what had previously been assumed to be irreversible disabilities." Alemtuzumab was developed in Cambridge and has been licensed for the treatment of chronic lymphocytic leukemia. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ June, 2008 FAMPRIDINE-SR INPROVES WALKING SPEED IN ALL TYPES OF MS IN SECOND PHASE 3 STUDY Walking speed improved significantly in a clinical trial of 240 people with all types of MS taking Fampridine-SR (MS-F204, Acorda Therapeutics, Inc.) compared with those taking inactive placebo. Fampridine-SR is a sustained-release formula of 4-aminopyridine, which temporarily enhances nerve signaling. These phase 3 study results were reported by Acorda in a press release dated June2, 2008. The company is planning to file for approval of this drug to treat mobility issues in MS in 2009. Problems with gait (difficulty in walking) are among the most common mobility limitations in MS. Fampridine-SR is a sustained-release formula of 4-aminopyridine, which blocks tiny pores, or potassium channels, on the surface of nerve fibers. This blocking ability may improve the conduction of nerve signals in nerve fibers whose insulating myelin coating has been damaged by MS. The first studies of this potassium-blocking approach in people with MS were supported by the National MS Society. In an earlier phase 3 study of 283 people with all types of MS, walking speed increased by 25% compared with placebo. Two serious adverse events led patients to discontinue Fampridine - one case of anxiety and one seizure in a person who developed sepsis from a urinary tract infection. (Abstract #S32.003, AAN 2007)
LAQUINIMOD RESULTS PUBLISHED: ORAL DRUG REDUCES DISEASE ACTIVITY IN PHASE 2 STUDY Treatment with oral laquinimod (Teva Pharmaceutical Industries) reduced disease activity by 40.4% compared with inactive placebo in a phase 2 study of 306 people with relapsing-remitting MS. Laquinimod is believed to affect the immune attack on the brain and spinal cord that occurs in MS. Giancarlo Comi, MD (Scientific Institute San Raffaele, Milan) and colleagues, who originally reported the results at the Annual Meeting of the American Academy of Neurology in 2007, now publish these results in the Lancet (2008; 371: 2085-92). A phase 3 study of laquinimod is underway on 1000 people with relapsing-remitting MS. Multiple sclerosis involves immune-system attacks against the central nervous system. Currently approved therapies for MS involve injections or infusions. Having an effective therapy on pill form would be a big step forward for people with MS. Laquinimod is an oral therapy that is thought to shift the balance of immune cells away from inflammation. The drug is related in structure to linomide, which showed early promise but in phase 3 clinical trials caused significant adverse events including cardiac toxicity. ____________________________________________________________________________________________________________ ____________________________________________________________________________________________________________ April, 2008 DISAPPOINTING RESULTS FROM TRIAL OF RITUXIMAB IN PRIMARY-PROGRESSIVE MS Drug did not achieve primary goal of slowing progression, sponsors still analyzing other outcomes. A study of intravenous rituximab (Rituxan, Genentech and Biogen Idec) in 439 people with primary-progressive MS has shown that the drug did not slow disease progression when compared with inactive placebo, the primary endpoint of the study. These results have been announced in a press release from Genentech and Biogen Idec dated April 14, 2008. The companies say that they will continue to analyze the data and will present the results at an upcoming medical meeting. "News" articles are derived from research releases made by the National MS Society |