You can also keep up to date with the latest in political MS news here Â and also news with regards MS Nurses World Wide

This page is updated daily with breaking news stories with regards to Multiple Sclerosis forÂ this month.

Introducing MS-UK

We did promise some changes for the New Year and would like to take this opportunity to bring you the very latest developments at the charity. For twenty years MSRC has supported people affected by multiple sclerosis; people are at the centre of everything we do and we are always looking for new and improved ways to present our services to those who need them. From 30th January, MSRC becomes Multiple Sclerosis UK or MS-UK. Our rebrand includes a brand new website â http://www.ms-uk.org/ which will be available from Wednesday 30th January. We will still offer a roundup of the latest MS news across the globe and all the information you have come to expect on our website but it will be easier to navigate with a host of new features. Our name and our logo may have changed but our core principles are still the same - to put people affected by MS at the very heart of our work and offer the best services we can in response to peopleâs needs. While we continue to get very positive feedback from those who use our services the truth is there are many people out there who donât know about us and the support we can offer. We need to reach them and those how are newly diagnosed. But if weâre going to be successful we must make sure that we have a clear message and that we, as an organisation, are easily recognisable. So, weâve made some changes! Gone is MSRC â we are now called MS-UK reflecting our national reach. Gone is the complicated round badge â in its place is a simplified yet dynamic logo. Weâre delighted to say that the charity has expanded rapidly over the last two years, with increases in staff and volunteers. This means that we can offer more services but we need to let specialists within the MS community â people like neurologists, GPs and MS nurses â know that weâre here. Our identity must reinforce the message that these specialists can have confidence in our team. So why the change? Simply put, to help us do more for those affected by MS. Here we look at the reasons behind the change and help you understand more about our new brand. If you have any questions or feedback, please get in touch at [email protected]. FAQs Q. Whatâs with the new name? A. Multiple Sclerosis Resource Centre no longer describes who we are or what we do. We know that because youâve told us via your feedback! MS-UK denotes that we are a national charity offering many services. As we enter our 20th year we need a name that reaches out to those newly diagnosed as well as to others affected by MS who may not know of our existence. Q. How did you come up with the new logo? A. One of our priorities was that the new logo must be noticed! Weâve therefore chosen lines that spread out, representing our reach to others and them reaching to us for support. The broken lines represent the breaks in the myelin sheath that are caused by MS. The strapline: âworking together to live life with MSâ sums up what we do â we are here to help people with MS live life to their fullest. Q. Does this mean you are changing your services? A. The rebrand will help us to communicate the full range and depth of our services. There will be no change to what core services we offer but there will be some improvements!



Many people are aware of some of our services but not about others. The rebrand will allow us to better communicate our services to more people. Some people just want advice or information, others may prefer counselling, some just like to receive the magazine, others prefer the website. MS-UK is about choice and people can choose which services they feel they need.



Firstly, weâve updated our website. The previous version was over a decade old (very elderly in website terms!) and simply could not keep up with the demands of modern technology. Weâve seen a 56% increase in users to our website over the past two years so we know how important it is for you to have a site thatâs accessible, easy to navigate and packed with information. Secondly, weâve given our magazine, New Pathways, a fresh new look but donât worry â youâll find the same features that you love inside and, of course, the name stays the same. Subscribing to New Pathways cost just Â£15 for a year (in the UK) â thatâs 6 issues delivered straight to your door. Find out more details by clicking here. Thirdly, our advisory team has grown and improved to include BACP counsellors. Over the next year we will be reviewing the service to make it better suited to those using the service. Finally, more titles will be added to our range of Choices leaflets. These provide in depth information about various aspects of living with MS. Q. Did it cost a lot of money? A. By rebrand standards, no. We kept costs low by doing a lot of work in house but we would also like to say thank you to Allistair Hunter from Direct Solutions who helped guide MS-UK through the process of managing the rebrand. Allistairâs advice and support has been invaluable and has saved the charity considerable costs.



We see the rebrand as a necessary investment that will take our charity to the next level. This will allow us to attract more funding, expand our services and provide even better support for anyone affected by MS. Q. Are you called Multiple Sclerosis UK or MS-UK? A. Our registered company name is Multiple Sclerosis-UK Limited. Our trading name is MS-UK so thatâs the name youâll see and hear. Our charity number and company number have not changed. Q. Does this affect my subscription to New Pathways? A. No. New Pathways magazine will have a fresher look that we hope will make it easier to read and appeal to a wider audience but thatâs the only change. If you pay by direct debit, you will now notice our name change on your bank statement. If you have a direct debit set up with us we will be writing to you. If you donât pay by direct debit at the moment, please consider setting one up. They are easy to use, 100% safe and this way you donât need to worry about forgetting to renew your subscription. Q. Is your rebrand in response to Chief Executive, Helen Yates-Motion, leaving? A. No. The timing of Helenâs leaving is coincidental. In fact, Helen started the ball rolling and was involved in the start of the rebranding process. She fully supports the project. Q. What will our supporters think about the rebrand? A. We are really excited about our new visual identity and we hope our supporters will be too. We are confident that this new way of identifying our charity, itâs goals and itâs services, will allow us to reach more people than ever before. Q. Can I still buy MSRC goodies? A. MSRC goods are still available until the 30th January â many at half price. Those at half price will never be seen again and only while stocks last. Visit our webshop at http://www.securio.net/msrc/ Q. How can I help? A. We really need your help to support our work and help spread awareness of MS and how MS-UK can offer support. Here are just a few ways in which you can get involved: â¢ Sign up for our free monthly e-newsletter by clicking here

â¢ Join our social community on Facebook and Twitter and help more people find out about what we do.

â¢ Give a monthly donation â however big or small, your donation will make a real difference to someone living with MS. Donate online at http://www.justgiving.com/msrc/donate or phone the office 01206 226500.

â¢ Subscribe to New Pathways our bi-monthly magazine here

â¢ Spread the news! Wear your MS-UK badge proudly (available from 30th January), arrange for your GPsâ surgery to stock our information leaflets or help to publicise one of our fundraising events. Thank you â your help means the world to us and to people affected by MS.

Applications for first-line use of Tysabri in anti-JCV antibody negative patients with MS announced

Biogen Idec and Elan Corporation, plc have announced that they have submitted applications to the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA) requesting updates to the TysabriÂ® (natalizumab) labels. The applications request an expanded indication that would include first-line use for people living with certain relapsing forms of multiple sclerosis (MS) who have tested negative for antibodies to the JC virus (JCV). A formal assessment of both applications is ongoing. These submissions are supported by risk stratification data and a risk algorithm that enables physicians and individuals living with MS to make informed decisions when considering treatment with Tysabri. If approved, a first-line label will allow all appropriate anti-JCV antibody negative patients to consider Tysabri early in the course of treatment, regardless of the level of disease activity or prior treatment history. TYSABRI is a highly efficacious treatment that has been shown to slow disability progression by 42 â 54 percent and reduce annualized relapse rates by 68 percent. âOur anti-JCV antibody test, STRATIFY JCVÂ®, helps to determine the most appropriate patients for TYSABRI and the data collected to date supports our recent filing for first-line use,â said Alfred Sandrock, M.D., Ph.D., senior vice president, Development Sciences and Chief Medical Officer, Biogen Idec. âMany appropriate patients are already benefiting from TYSABRI. A first line approval would allow people with MS access to a highly efficacious treatment earlier in the course of the disease, potentially leading to better outcomes. This is an important consideration for people with MS who may want or need more efficacy.â Currently in the U.S., due to an increased risk of an opportunistic viral infection, progressive multifocal leukoencephalopathy (PML), Tysabri is generally recommended for people living with relapsing forms of MS whose disease is not responding to, or who are unable to tolerate, an alternative therapy regardless of JCV status. In the EU, TYSABRI is approved for highly active relapsing-remitting MS (RRMS) in adult patients who have failed to respond to beta interferons or have rapidly evolving, severe RRMS. âTysabri is an important treatment option for thousands of people living with MS,â said Hans Peter Hasler, chief operating officer, Elan Corporation, plc. âWe are excited about these filings and the potential to make TYSABRI available as a treatment option for more individuals early in the course of their disease.â Source: Business Wire Â© 2010 - 2012 Postmedia Network Inc. (16/01/13)

Multiple sclerosis takes Scott Mills' sidekick off air

After five years working on air with Scott Mills, Beccy Huxtable is leaving her role on the Radio 1 afternoon show. She was diagnosed with multiple sclerosis in 2012 but hasn't spoken about it on the radio until now. "I think it was important that people knew why I was going," she said. "If I can raise a bit of awareness, then that's all for the better. "You don't want it to rule your life, so I'm going to make positive changes to stop it affecting me." Role change

Beccy will continue to work as an assistant producer for the BBC network but will take on more responsibilities off air rather than on. She admits it wasn't an easy decision to take, stressing that "working on Scott's show is brilliant" and that she "absolutely loves it". However, she says the practicalities of the disease made her review her daily working. "On a day-to-day radio show there are so many deadlines it's really hard and sometimes if I wake up and I can't walk properly or can't get into work on time, that makes it awkward for everybody. "I know they've been really supportive but it would make me feel much better if I could go, 'actually I'm going to work from home today,' or 'I'm going to come in later'." Leaving do Scott Mills says he's sad to see his 'mate' Beccy leave the show. "At the end of the day you need to look after her health first of all and that's what hopefully her new role will do. "And I still get to work with her at Radio 1, it's not like she's going very far so that consoles me a little." Becky's final day on air as part of Scott Mill's team will be Friday 18 January but the Radio 1 presenter says he has plans in place. "Imagine the Olympics opening ceremony and then think a lot smaller. "But it's going to be good, I've been working quite hard on it myself actually, for once." Source: BBC Â© 2013

New research network for multiple sclerosis research

European Commission to contribute approximately EUR 3.5 million for network development spearheaded by the Mainz University Medical Center To date, Multiple Sclerosis (MS) has been considered to be an incurable disease involving the immune system and its exact causes are still unknown. Why exactly is there inadequate communication between the various kinds of immune cells in patients with the autoimmune disease MS? Why are the brains of MS patients the targets of "accidental" attacks by their own immune system? It is hoped that the research network ITN-NeuroKine, currently in the process of being formed under the aegis of the University Medical Center of Johannes Gutenberg University Mainz (JGU) with the help of EUR 3.5 million in funding provided by the European Commission, will provide answers to these questions. ITN stands for Initial Training Network, a concept established as one of the Marie Curie Actions and designed to promote European networks for the structured training of young researchers. 'NeuroKine' is an acronym for 'Neurological disorders orchestrated by cytoKines'. The ITN NeuroKine network was launched on January 1, 2013. "The core objective of our new ITN-NeuroKine research network is to gain insight into the impairment of communication between immune cells," explained Professor Dr. Ari Waisman, Director of the Institute of Molecular Medicine (IMM) at the Mainz University Medical Center. "We will specifically be focusing on the soluble proteins called cytokines, which regulate the communication between these cells." Immune cells are mobile and are present at various sites in the body. The ITN-NeuroKine research network is composed of an international team of researchers with a broad range of expertise in the areas of molecular and cellular neuroimmunology and neuropathology. The participants are scientists from the University of ZÃ¼rich (UZH), the Medical University of Vienna (MUW), the Parisian Institut National de la SantÃ© et de la Recherche MÃ©dicale (INSERM), the UniversitÃ Vita-Salute San Raffaele (USR) in Milan, the Weizmann Institute of Science (WIS) based in Rehovot, Israel, the Erasmus University Medical Center in Rotterdam (EMC), and the CharitÃ© University Hospital in Berlin together with various commercial medical organizations, such as Miltenyi Biotech GmbH, Apitope Technology Ltd., Phenex Pharmaceuticals AG, and the Mainz-based BioNTech AG. Also participating are the Postdoc Career Development Initiative (PCDI) in Utrecht, the Novartis Institutes for BioMedical Research in Basel, and GlaxoSmithKline. "The creation of the ITN-NeuroKine research network is crucial to the reputation of Mainz as a science hub. On the one hand, the ITN-NeuroKine network will be conducting cutting-edge research into the area where brain and immune system interact. At the same time, this network will be providing young researchers with the opportunity to receive specialized training," emphasized Professor Dr. Dr. Reinhard Urban, Chief Scientific Officer of the Mainz University Medical Center. Source: Eureka Alert Copyright Â©2013 by AAAS, the science society (15/01/13)

Stem Cell study offers hope to multiple sclerosis patients

Scientists in recent years have found a way to infuse stem cells into the brains of animals to repair damage to the central nervous system, offering some of the most encouraging news yet for multiple sclerosis patients. Now, a key $12.1 million study soon will be under way in Buffalo and two other upstate medical centers that will for the first time begin to test the procedure in people. The hope is that the stem cells will generate new myelin, the fatty substance that surrounds nerves like the insulation on a wire. Myelin is damaged in MS, leading to weak or lost signals between nerves. Eventually, the painful disease spreads in a slow, unpredictable path toward paralysis. âThis is a promising strategy. It has been extraordinarily effective in mice, and there is great hope the technique will be successful in people,â said Dr. Steven Goldman, co-principal investigator and co-director of the University of Rochester Center for Translational Neuromedicine. The study by researchers in Rochester, the University at Buffalo and Upstate Medical University in Syracuse has far-ranging implications. It potentially could be applied to millions of patients with a host of other conditions, including Alzheimerâs and Parkinsonâs disease. Although stem cells show great promise, the approach is a ways from reality. What works in mice does not always work in humans. In addition, scientists donât know what causes MS, so they canât exactly replicate MS in animals, complicating tests of the potential new treatment. âExpectations have to be kept under control. Youâre not going to implant stem cells in people and suddenly see them running around,â said Dr. Bianca Guttman-Weinstock, co-principal investigator at UB. Stem cells are often referred to as master cells because they develop into the many different types of cells in the body that form organs and tissue. Stem cells also have the potential to repair or replace damaged cells. Other scientists are looking at whether it may be possible to use certain stem cells to prevent the bodyâs immune system from attacking nerves. âThere is a lot happening in stem cell research, and itâs exciting because five years ago, these were just ideas. Now, they are reality,â said Dr. Timothy Coetzee, chief research officer at the National MS Society. Until recently, scientists didnât know exactly which master stem cells ultimately developed into cells that make myelin in a complicated process. They now know that cells called oligodendrocytes produce myelin. They also learned how to turn stem cells into a type of cell called glial progenitor cells. Glial progenitor cells are the cells that make oligodendrocytes. These findings allowed scientists to transplant oligodendrocytes into the brains of mice that had no myelin. The result: The cells began to repair damaged areas. âIt was an extraordinarily effective strategy,â said Goldman. All this progress has occurred in the last few years, including a study published late last year using stem cells transplanted into the brains of children with a rare genetic brain disease known as Pelizaeus-Merzbacher disease, in which myelin is lacking. The significance of the research is that it indicates stem cells can be safely transplanted and may be effective at making myelin. Children are different than adults, but Goldman and others say there is great hope the technique will succeed in adults. The first step

The upstate consortium study for MS, which is funded by the Empire State Stem Cell Board, is the first step in a typical research process, which occurs in phases and usually takes many years to complete. In the first two phases, scientists test the safety and effectiveness of an experimental treatment, and thatâs what will happen with this stem cell trial for MS. Patients enrolled in the study will be those with secondary progressive MS. These individuals no longer have periods of remission and, instead, experience a slow but steady worsening of symptoms with no approved therapy. Small holes will be drilled into their skulls and stem cells injected through catheters inserted in the holes. The original proposal for the study recommended obtaining stem cells from discarded fetal brains. Technology has progressed enough that the current plan, dependent on government approval, is to start with stem cells from the patientâs own skin cells and reprogram them into cells useful for making myelin. Before the first patients can receive the treatment in 2016, researchers must spend the next few years preparing for the trial. Among other things, they need to refine how they will measure the repair of myelin, as well as improvements in the patients. Itâs a tricky issue because improvements are likely to occur slowly and will vary from person to person, said Guttman-Weinstock. A key role

It seems fitting that the study will include Buffalo. Research by the late Dr. Lawrence D. Jacobs, a Buffalo neurologist, played a key role in the development of Avonex, the drug most widely prescribed to treat relapsing MS. Population studies show that higher rates of MS exist in temperate climates, in particular a geographic band in North America across the northern United States and southern Canada that includes Western New York. If stem cells work, it could change the lives of millions of people worldwide who suffer from a disease that can be unbearable as patients decline in function and health. Thatâs why many individuals like Shelly Boyle track research on potential MS treatments with a laser-like focus. âI read everything I can read,â said Boyle, a 48-year-old Cheektowaga resident who was diagnosed with MS in 1990. She stopped working as a chiropractor in 2004 as her symptoms worsened. She has trouble walking and coordinating the small muscles in her fingers. The medication she has been taking is no longer effective. âThe idea of drilling into my brain would scare me if I was in the trial, but the prospect of something new on the horizon is exciting,â she said. âIâm running out of options.â Source: The Buffalo News Copyright 1999 - 2013 - The Buffalo News (14/01/13)

MS study reveals how killer T cells learn to recognise nerve fibre insulators

Misguided killer T cells may be the missing link in sustained tissue damage in the brains and spines of people with multiple sclerosis, findings from the University of Washington reveal. Cytoxic T cells, also known as CD8+ T cells, are white blood cells that normally are in the bodyâs arsenal to fight disease. Multiple sclerosis is characterized by inflamed lesions that damage the insulation surrounding nerve fibers and destroy the axons, electrical impulse conductors that look like long, branching projections. Affected nerves fail to transmit signals effectively. Intriguingly, the UW study, published this week in Nature Immunology, also raises the possibility that misdirected killer T cells might at other times act protectively and not add to lesion formation. Instead they might retaliate against the cells that tried to make them mistake the wrappings around nerve endings as dangerous. Scientists Qingyong Ji and Luca Castelli performed the research with Joan Goverman, UW professor and chair of immunology. Goverman is noted for her work on the cells involved in autoimmune disorders of the central nervous system and on laboratory models of multiple sclerosis. Multiple sclerosis generally first appears between ages 20 to 40. It is believed to stem from corruption of the bodyâs normal defense against pathogens, so that it now attacks itself. For reasons not yet known, the immune system, which wards off cancer and infection, is provoked to vandalize the myelin sheath around nerve cells. The myelin sheath resembles the coating on an electrical wire. When it frays, nerve impulses are impaired. Depending on which nerves are harmed, vision problems, an inability to walk, or other debilitating symptoms may arise. Sometimes the lesions heal partially or temporarily, leading to a see-saw of remissions and flare ups. In other cases, nerve damage is unrelenting. The myelin sheaths on nerve cell projections are fashioned by support cells called oligodendrocytes. Newbornâs brains contain just a few sections with myelinated nerve cells. An adultâs brains cells are not fully myelinated until age 25 to 30. For T cells to recognize proteins from a pathogen, a myelin sheath or any source, other cells must break the desired proteins into small pieces, called peptides, and then present the peptides in a specific molecular package to the T cells. Scientists had previously determined which cells present pieces of a myelin protein to a type of T cell involved in the pathology of multiple sclerosis called a CD4+ T cell. Before the current study, no cells had yet been found that present myelin protein to CD8+ T cells. Scientists strongly suspect that CD8+ T cells, whose job is to kill other cells, play an important role in the myelin-damage of multiple sclerosis. In experimental autoimmune encephalitis, which is an animal model of multiple sclerosis in humans, CD4+T cells have a significant part in the inflammatory response. However, scientists observed that, in acute and chronic multiple sclerosis lesions, CD8+T cells actually outnumber CD4+ T cells and their numbers correlate with the extent of damage to nerve cell projections. Other studies suggest the opposite: that CD8+T cells may tone down the myelin attack. The differing observations pointed to a conflicting role for CD8 + T cells in exacerbating or ameliorating episodes of multiple sclerosis. Still, how CD8+T cells actually contributed to regulating the autoimmune response in the central nervous system, for better or worse, was poorly understood. Goverman and her team showed for the first time that naive CD8+ T cells were activated and turned into myelin-recognizing cells by special cells called Tip-dendritic cells. These cells are derived from a type of inflammatory white blood cell that accumulates in the brain and the spinal cord during experimental autoimmune encephalitis originally mediated by CD4+ T cells. The membrane folds and protrusions of mature dendritic cells often look like branched tentacles or cupped petals well-suited to probing the surroundings. The researchers proposed that the Tip dendritic cells can not only engulf myelin debris or dead oligodendrocytes and then present myelin peptides to CD4 + T cells, they also have the unusual ability to load a myelin peptide onto a specific type of molecule that also presents it to CD8+ T cells. In this way, the Tip dendritic cells can spread the immune response from CD4+ T cells to CD8+ T cells. This presentation enables CD8+ T cells to recognize myelin protein segments from oligodendrocytes, the cells that form the myelin sheath. The phenomenon establishes a second-wave of autoimmune reactivity in which the CD8+ T cells respond to the presence of oligodendrocytes by splitting them open and spilling their contents. âOur findings are consistent,â the researchers said, âwith the critical role of dendritic cells in promoting inflammation in autoimmune diseases of the central nervous system.â They mentioned that mature dendritic cells might possibly wait in the blood vessels of normal brain tissue to activate T-cells that have infiltrated the blood/brain barrier. The oligodendrocytes, under the inflammatory situation of experimental autoimmune encephalitis, also present peptides that elicit an immune response from CD8+T cells. Under healthy conditions, oligodendrocytes wouldnât do this. The researchers proposed that myelin-specific CD8+T cells might play a role in the ongoing destruction of nerve-cell endings in âslow burningâ multiple sclerosis lesions. A drop in inflammation accompanied by an increased degeneration of axons (electrical impulse-conducting structures) coincides with multiple sclerosis leaving the relapsing-remitting stage of disease and entering a more progressive state. Medical scientists are studying the roles of a variety of immune cells in multiple sclerosis in the hopes of discovering pathways that could be therapeutic targets to prevent or control the disease, or to find ways to harness the bodyâs own protective mechanisms. This could lead to highly specific treatments that might avoid the unpleasant or dangerous side effects of generalized immunosuppressants like corticosteroids or methotrexate. The study was funding by grants AI072737 and AI073748 from the National Institutes of Health. The authors declared no competing financial interests. Source: University of Washington Â© 2013 UNIVERSITY OF WASHINGTON (11/01/13)

Identifying the molecular causes of vision loss in demyelinating disease

Demyelinating diseases, such as multiple sclerosis (MS), are frequently associated with the progressive loss of vision. The retinal nerve damage is thought to be caused by immune system-mediated inflammation; however, other demyelinating disorders, such as Pelizaeus-Merzbacher disease, do not involve the immune system, suggesting that there are other causes of retinal nerve damage. Deimination is a protein modification that is altered in patients with MS and PMD. In this issue of the Journal of Clinical Investigation, researchers led by Sanjoy Bhattacharya at the University of Miami investigated the role of deimination in retinal nerve damage in a mouse model of demyelinating disease (ND4 mice). They found that deimination was reduced in patients with demyelinating diseases and in ND4 mice that exhibited vision loss. Decreases in deamination could be detected in the mice prior to the onset of other symptoms. Bhattacharya and colleagues found that they could improve visual function in ND4 mice by restoring deimination. These results demonstrate that loss of deimination underlies nerve damage in demyelinating diseases and may be a suitable target for therapeutic intervention. Source: Medical News Today Â© MediLexicon International Ltd 2004-2013 (08/01/13)

FDA approves Rebif Rebidose interferon beta-1a for Multiple Sclerosis

Merck Serono, a division of Germany's Merck, announced that the U.S. Food and Drug Administration (FDA) approved Rebif(R) Rebidose(R) (interferon beta-1a), a single-use auto-injector for the self-administration of Rebif, a disease-modifying drug used to treat relapsing forms of multiple sclerosis (MS). Rebif Rebidose was evaluated in a 12-week Phase IIIb multicenter, open-label, single-arm study for the self-administration of Rebif with respect to ease of use, patient satisfaction and acceptability, and functional reliability. In the trial, patients with relapsing MS, who were receiving Rebif 44 microgram three times weekly for more than 12 weeks, continued MS therapy using Rebif Rebidose for 12 weeks. The results of the trial showed that the majority of patients found the device easy to use. Rebif RebiDose was designed with the objective to assist with ease of use and to offer patients an alternative delivery option. In the US, it will be available in a monthly pack in two different doses, 22 micrograms and 44 micrograms, and in a titration pack. Rebif RebiDose was launched in Europe in 2010 and it will be available in the U.S. in early 2013. With this approval, all three delivery options of Rebif (prefilled syringes, Rebiject II and Rebif RebiDose) will be available in the U.S. to provide a range of options to meet the needs of patients treating their relapsing forms of MS with Rebif. "Over the past two decades, treatment of relapsing MS has advanced substantially, and Rebif has remained an established treatment option," said Belen Garijo, Head of Global Operations at Merck Serono. "We are committed to invest in valuable incremental innovations developed to bring additional value for the patient." Source: Science 2.0 Â© 2013 ION Publications LLC (04/01/13)

Researchers identify immune cells that may contribute to the development of MS

Multiple sclerosis (MS) is characterised by the infiltration of the central nervous system (CNS) by immune cells. A particular type of immune cell, Tc17, has been found in MS lesions in humans, but it is unclear what role these cells play in disease pathogenesis. In the Journal of Clinical Investigation, researchers led by Magdalena Huber at the University of Marburg in Germany used a mouse model of MS to determine the role of Tc17 cells. They found that Tc17 cells help Th17 immune cells to invade the CNS by secreting the protein IL-17. Without Tc17 cells, the Th17 cells did not accumulate in the CNS, preventing the development of MS. This study demonstrates that Tc17 cells help initiate MS by allowing immune cells to reach the CNS and suggests that therapies targeting Tc17 cells might be helpful in treating early MS. Article: IL-17A secretion by CD8+ T cells supports Th17-mediated autoimmune encephalomyelitis Source: Science Codex (02/01/13)

New eye scan found helpful in diagnosis of multiple sclerosis patients

A simple, non-invasive eye test could offer a way to measure how fast multiple sclerosis is progressing in a patient. The scan, known as Optical Coherence Tomography (OCT), takes just a few minutes per eye and can be performed at a GPs surgery. Researchers from John Hopkins University performed scans on 164 M.S. patients, measuring the thickness of the lining at the back of the eye. It was determined that patients with thinning of the retina had both earlier and more active forms of the disease. Fifty-nine of the patients showed no symptoms. All patients received exams for six months for around 21 months. They also gave them MRI brain scans once a year. Multiple sclerosis is a disease that affects nerves in the brain and spinal cord, causing problems with muscle movement, balance and vision. Around eight out of 10 people with M.S. have a type known as relapsing remitting. People will have periods where symptoms are mild or disappear altogether followed by flare-ups with this version of the disease. After around 10 years, half of patients will develop secondary progressive disease where symptoms get worse, with little remission. Monitoring the disease is highly difficult because its course can be unpredictable. Scientists believe OCT could provide a good way to do this. "As more therapies are developed to slow the progression of MS, testing retinal thinning in the eyes may be helpful in evaluating how effective those therapies are," study author Dr Peter Calabresi says. The study found that people with MS relapses had 42 percent faster thinning than people with MS who had no relapses. In addition, the MRI scans revealed people with MS who had signs of active inflammation, such as gadolinium-enhancing lesions experienced 54 percent faster thinning. Patients, in the meantime whose level of disability worsened during the study experienced 37 percent more thinning than those who had no changes in their level of disability. The study was supported by the National Multiple Sclerosis Society, the National Eye Institute and Braxton Debbie Angela Dillon and Skip Donor Advisor Fund. Source: Catholic Online Copyright 2012 Catholic Online (27/12/12)

FDA clears startup's virtual trial for drug against multiple sclerosis

Transparency Life Sciences picked up a win for its bet on open innovation in transforming drug development. The FDA cleared the developer's IND application to study a generic hypertension drug for a new potential use in patients with multiple sclerosis, after the startup tapped crowdsourced input from experts and patients on aspects of the clinical trial. The study not only used New York-based Transparency's web-based Protocol Builder software to gather ideas on the design of the Phase II effort, but the trial will also be partially virtual. After patients' initial visits to trial sites, the planned 12-month study is expected to use telemonitoring technology from Advanced Monitored Caregiving and other partners to track participants until their final checkups, COO Marc Foster explained to FierceBiotechIT. With these outside-the-box strategies, Transparency aims to drive down the cost of clinical trials by at least 50%. This is a big goal and one not easily achieved industry-wide, and at first blush, the startup's bold idea might draw some healthy skepticism. As published in a Nature Reviews Drug Discovery article in March, the number of FDA approvals per billion dollars in research money spent has been steadily declining over the past 60 years or so. The authors dubbed this "Eroom's Law," which is Moore's Law spelled backwards. Transparency's Foster believes there is hope for reversing the troubling trend. "I think it's doable. It takes a fresh approach. It takes a bold approach," Foster said in a phone interview. "Just tinkering with the status quo is not working, and it's really resulted in an unsustainable clinical development model that has translated into escalating costs." How does Transparency expect to drastically reduce the cost of clinical research? For starters, the company is crowdsourcing patients and healthcare experts to augment its reliance on internal thought leaders to design trial protocols. Its hope is to show that this is an efficient and effective approach to protocol design, which can take substantial time and money to complete In the MS study, the company wants to trial a new use of a widely prescribed generic heart drug in the ACE inhibitor lisinopril, which has a well-established safety profile that allows the startup to begin its program with a midstage study. (A company co-founder documented the generic drug's benefits for MS in animal studies, resulting in a new method of use patent filing.) Foster also aims to get discounted supplies of the drug from generics companies. Overall, he sees an opportunity to pick up drugs that are ready for Phase II from around the industry, using the company's open innovation approach to reduce development costs of the molecules, with plans to license successful candidates to partners after midstage studies. The partners would foot the hefty bills for Phase III trials. The company has found a lead investigator at Stanford who treats many MS patients, and Foster sees an opportunity to cut recruitment costs by enrolling all the estimated 150 to 180 study participants from the San Francisco Bay Area. Recruitment is notoriously expensive, and drawing from the investigator's large pool of patients for the study could significantly reduce that expense. The next bucket of savings is expected to come from reduced clinical monitoring costs because participants will self-report their status from their homes with mobile devices for most of the study, reducing the cost of traveling to clinics with high costs of doing business, Foster says. Transparency is considering a GPS-enabled system to provide remote monitoring of MS patients' movements, as their neurological disorder causes progressive disability. Transparency is taking a hybrid approach to virtual clinical development that might just work. We'll keep track of its progress. Source: FierceBiotechIT Â© 2012 FierceMarkets (20/12/12)

New molecular test in clinical trials could help physicians identify MS earlier