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    Latest MS News

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    Latest Multiple Sclerosis NewsThis page is updated daily with breaking news stories with regards to Multiple Sclerosis for this month.

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

    You can subscribe to our Latest MS News RSS Feed by clicking here: MSRC Latest MS News RSS Feed

    N.B. MS News stories for the previous 12 months can be accessed in the MS News Archive

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

    T CellsMisguided 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 body’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 body’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. Newborn’s brains contain just a few sections with myelinated nerve cells. An adult’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.

    “Our findings are consistent,” the researchers said, “with the critical role of dendritic cells in promoting inflammation in autoimmune diseases of the central nervous system.” 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 wouldn’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 “slow burning” 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 body’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 © 2013 UNIVERSITY OF WASHINGTON (11/01/13)

    Identifying the molecular causes of vision loss in demyelinating disease

    EyeDemyelinating 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 © MediLexicon International Ltd 2004-2013 (08/01/13)

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

    RebidoseMerck 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 © 2013 ION Publications LLC (04/01/13)

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

    T CellsMultiple 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

    EyesA 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

    NeuronsTransparency 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 © 2012 FierceMarkets (20/12/12)

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

    B CellsAbout 2.5 Million people worldwide have multiple sclerosis, a chronic central nervous system disease that can cause blurred vision, poor coordination, slurred speech, numbness and paralysis, among other things.

    Despite the serious symptoms, diagnosis is often tricky because symptoms vary and can be hard for physicians to interpret. Gaithersburg, Maryland company DioGenix Inc. started up in 2008 to commercialize work on a lab test that could improve the diagnostic process.

    A 150-patient clinical trial has just begun enrolling, the trial will validate its test, MS Precise, for early identification and diagnosis of multiple sclerosis.

    Multiple sclerosis is characterised by scarring of the myelin sheath in nerve cells that disrupts the transmission of messages from the brain and causes inflammation. Because MS signs and symptoms are also characteristic of other nervous system disorders, the disease is typically diagnosed through a deductive process that includes medical history, physical exams, an MRI and analysis of spinal fluid.

    The analysis of spinal fluid typically looks for evidence of general inflammation that’s not seen in the blood, DioGenix CEO Larry Tiffany said. But even that can’t give a definitive diagnosis and produces false positives. According to the Multiple Sclerosis Foundation, diagnosis is correct 90-95 percent of the time.

    DioGenix’s lab test takes the cerebral spinal fluid test a step further, looking for gene mutations in certain spots within the B-cell genome that research has suggested are driven specifically by MS. Tiffany said the team thinks the specificity of the test could help clinicians distinguish MS from other immune-mediated neurological diseases that share similar biological features. It may also someday be able to help physicians identify more aggressive cases of MS.

    In a recent study, the test outperformed the current method of analysis in patients suspected of having MS, according to the company. A more confident diagnosis would hopefully lead to better use of prescription of MS drugs, which suppress or alter the immune system and shouldn’t be used by people without the condition.

    DioGenix’s test is an extension of the work of Dr. Nancy Monson’s team at the University of Texas Southwestern Medical Center. A blood test based on the same technology is also in development.

    Source: MedCity News Copyright 2012 MedCity News. (19/12/12)

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