research

Propionic acid supplements alter the composition and behavior of immune cells in multiple sclerosis (MS) patients — likely by changing the composition of gut bacteria, according to Alexander Duscha from Ruhr University Bochum in Bochum, Germany. The finding, presented Wednesday at the 7th Joint ECTRIMS-ACTRIMS Meeting running in Paris…

The numbers of people being diagnosed with multiple sclerosis is rising worldwide, though distinct differences in factors thought to drive this rise are evident among regions, according to MS data represented by researchers on patients in Asia, Latin America, and the Australia-New Zealand. The data was part of the session “Prevalence and…

Opicinumab, an investigative treatment aiming to promote remyelination in relapsing multiple sclerosis (MS) patients, will be tested in a new clinical trial —  having failed at an earlier effort, but having shown promise enough in particular patients to be worth a closer look. In fact, the new AFFINITY study “is…

There’s been some internet buzz recently about the possibility of an over-the-counter allergy drug that helps to repair the myelin that MS damages. The drug is clemastine fumarate, and I suspect that some of that buzz may have been generated by headlines found on Twitter and…

Atara Biotherapeutics has started a Phase 1 clinical trial to assess ATA188’s safety and potential to treat progressive or relapsing-remitting multiple sclerosis. ATA188 is the company’s next-generation T-cell immunotherapy. It targets Epstein-Barr virus antigens that play an important role in the development of MS. An antigen is a molecule capable of…

An immune signaling protein called interleukin-35 has anti-inflammatory properties that scientists might harness to develop a therapy for multiple sclerosis and other autoimmune disorders, according to two studies. Researchers at the National Eye Institute of the National Institutes of Health discovered that a subunit of interleukin 35, which is also known as IL-35, significantly reduced inflammation in mouse models of eye inflammation and multiple sclerosis. Immune B-cells produce IL-35 to communicate with, and regulate the behavior of, surrounding cells. In a previous study, the research team found that the protein could inhibit inflammation in the eyes of animals with autoimmune uveitis, or inflammation of the inner layers of the eye. An autoimmune disease is one in which the immune system attacks healthy cells instead of invaders. A drawback of trying to use a synthetic version of IL-35 as a therapy is that it's difficult to produce because of its complex structure and it's unstable in a solution. Natural IL-35 is composed of two subunits, IL-12p35 and Ebi3, which bind to create the full protein. The team wondered if they could use a subunit, instead of the full protein, as an anti-inflammatory agent. Their study, “IL-12p35 induces expansion of IL-10 and IL-35-expressing regulatory B cells and ameliorates autoimmune disease,” was published in the journal Nature Communications, They demonstrated that the IL-12p35 subunit could generate anti-inflammatory effects similar to those of the full IL-35 protein. Giving IL-12p35 to mice with uveitis promoted the expansion of immune B-cells that counteract autoimmune responses, reversing the animals' eye symptoms. In the second study, researchers discovered that the subunit tempered inflammation in a mouse model of multiple sclerosis. Giving the animals IL-12p35 every other day for up to 12 days promoted immune cell proliferation that inhibited inflammation in the mice's brains and spinal cords, improving their symptoms. The research demonstrated IL-35 and its subunit's potential to treat nerve-inflammation disorders. The team published its findings in the journal Frontiers of Immunology. The article is titled “IL-12p35 inhibits neuroinflammation and ameliorates autoimmune encephalomyelitis.” The team is now looking at IL-12p35's ability to treat other degenerative eye diseases, such as diabetic retinopathy and macular degeneration.

In its work on multiple sclerosis (MS), Biogen has adopted a comprehensive approach that ranges from  drug development to the exploration of real-world data and digital markers of disease. The company will showcase these efforts at the 7th Joint ECTRIMS-ACTRIMS Meeting in Paris on October 25–28. Among its more than 80 presentations at the meeting are updates from its collaboration with Verily and Brigham and Women’s Hospital on using digital sensors that gather data on MS patients between physician visits. Biogen will also share data on the possibility of using such biomarkers to help neurologists in diagnosing and following MS patients — offering information that could potentially help them in making treatment decisions given the variability of the disease in MS patients. The company is also involved in a collaboration with 10 MS centers that aims to generate data collected during routine care. The MS PATHS study includes data from physical examinations, magnetic resonance imaging (MRI) scans, and biological samples. A third and similar project — the Big Multiple Sclerosis Data (BMSD) Network —  is merging data from five MS registries, holding prospective information on nearly 140,000 patients. Taken together, these large collections of high-quality, real-world data will help researchers better understand the disease, and so, increase the potential of new treatment discoveries, Biogen says. The company is also working to discover and develop biomarkers that are not digital that may also advance the understanding of MS and its treatment. One such marker is neurofilament light, which signals damage to neuronal axons. Biogen will share data on how this marker changes over time in MS patients. Among presentations focusing on treatment development, Biogen will highlight new efforts with opicinumab . The treatment — intended to repair damage by triggering remyelination — failed to reach it primary goal in the Phase 2 SYNERGY trial earlier this year. Still,  data indicated that some trial participants did respond to the treatment. At ECTRIMS, Biogen will present an analysis of the SYNERGY data that identifies factors — including specific MRI features — that may be linked to a treatment response.  

New data on how Lemtrada and Aubagio perform in a real-world setting will be the focus of Sanofi Genzyme when the company showcases its research at the upcoming 7th Joint ECTRIMS-ACTRIMS Meeting in Paris this week. Researchers will also share information about the safety of a new investigational therapy, GLD52 (GZ402668), currently in a Phase 1 safety study. The TOPAZ study is one of the main data sources for the upcoming presentations. The study, which follows relapsing MS patients who participated in the CARE MS-I and CARE MS-II extension study , is a rich source of information on long-term outcomes. Researchers will share various aspects of disease outcomes and magnetic resonance imaging (MRI) data from patients followed up to seven years, with some presentations focusing solely on those who switched from treatment with interferon beta-1a. Among the Lemtrada highlights are findings demonstrating that Lemtrada does not appear to trigger birth defects. Another presentation compared Lemtrada to Genentech’s Ocrevus using a model that evaluated both the cost and effectiveness of the two drugs. The analysis suggests that Lemtrada more effectively treated relapsing MS and was also linked to lower costs over a 20-year period. Aubagio studies also focused on long-term patient data, including in people with progressive forms of relapsing MS. Data from the Phase 3 TEMSO , TOWER , and the TEMSO extension showed that Aubagio stabilized disability progression in these patients over nearly a decade. Other presentations homed in on Aubagio’s ability to slow brain tissue loss and improve cognitive outcomes. Finally, Sanofi Genzyme shared initial data on its investigational antibody GLD52. The treatment is an updated form of Lemtrada, which scientists believe gives rise to fewer and milder infusion-related reactions. Data from the Phase 1 study , so far indicated that this might indeed be the case, as no severe reactions occurred in the 44 progressive MS patients in the trial. For a complete list of Sanofi Genzyme's presentations at the meeting, visit this link.

Alkermes will showcase its work in developing a treatment that harnesses the effect of Tecfidera (dimethyl fumarate) for relapsing multiple sclerosis (MS), while lowering the risk of stomach problems at the 7th Joint ECTRIMS-ACTRIMS Meeting this month in Paris. The investigational drug, ALKS 8700, uses the same mechanism of action as Tecfidera. By building the molecule in a different way, however, the company expects it will show better tolerability. Once in the body, dimethyl fumarate turns into monomethyl fumarate (MMF), the molecule that actually impacts MS disease processes. But before giving rise to MMF, dimethyl can cause side effects in users, particularly gastrointestinal. In fact, stomach problem were what caused people in Tecfidera Phase 3 trials to stop the treatment. Alkermes uses a so-called prodrug approach to try to overcome this problem. By attaching a different compound to MMF — which breaks away from the molecule once in the body —  it is possible to deliver MMF with lesser gastrointestinal side effects, Phase 1 study data indicate. At the meeting, the company will present two posters on two clinical trials exploring ALKS 8700 in patients with relapsing-remitting MS. The first presentation, will describe a Phase 3 trial that aims to compare ALKS 8700 to Tecfidera in about 420 patients. The trial is primarily concerned with the drug’s safety, and will measure the occurrence and impact of gastrointestinal side effects in the two treatment groups. The presentation will only include descriptions of patients characteristics and study design, as outcomes are yet to be analyzed. Patients who complete the Phase 3 trial will be eligible to continue in an ongoing open-label, long-term safety study, called EVOLVE-MS-1, covered in the company’s second presentation. By March 3, 2017, the study had enrolled 543 patients. In addition to describing patient characteristics, researchers will present the rates of discontinuation caused by gastrointestinal adverse events within one month of starting the treatment.

Inhibiting an enzyme prevented mice from developing a multiple sclerosis-like disease, a European study reports. The finding about HDAC1, a member of the histone deacetylases family of enzymes, could open up new therapy possibilities for MS. Researchers published their study, “A T cell-specific deletion of HDAC1 protects against experimental…

TG Therapeutics’ ublituximab nearly eradicated a type of immune B-cell believed to be involved in multiple sclerosis, according to a Phase 2 clinical trial. The result was that none of the patients had a relapse during the first six months of the trial, which is continuing, researchers said. In addition, ublituximab reduced the brain and spinal cord lesions of the relapsing MS patients involved in the trial and prevented new ones from forming. The company will present the interim trial results in three poster presentations at the 7th Joint ECTRIMS-ACTRIMS Meeting in Paris, Oct. 25-28. Meanwhile, researchers will continue to study the effectiveness of ublituximab, a B-cell-depleting antibody, versus a placebo, for another six months. The trial is being held at several U.S. medical facilities. Participants receive two initial infusions of ublituximab or a placebo on day 1 and 15 during the first 28 days. After this initial period, those in the placebo-group are also given ublituximab and followed for 52 weeks. A key trial finding was that over the initial 24 weeks of the trial, the treatment nearly wiped out a type of B-cell known as CD20 that scientists believe is involved in the development of MS. Only 1 percent of the B-cells remained after a month. While helpful immune T-cell numbers dropped slightly after the first ublituximab infusion, they bounced back quickly. Researchers also reported a reduction in patients' magnetic resonance imaging (MRI) lesions, with no new inflammatory lesions appearing during the six months. So far, none of the trial participants has had a serious adverse event. Most of the adverse events were mild or moderate and related to the infusions. The trial also demonstrated that speeding up infusions did not increase infusion-related reactions. The speed-up results indicated that — if proven effective and safe — ublituximab will be more convenient for patients than B-cell-depleting drugs that require infusions stretching over several hours.

I have every single malady associated with MS. I’m absolutely positive. Because whenever I find out about a new one, or a new study that says we don’t sleep well, or we twitch or tremble, or suffer from this deficiency or that, I’ve got it.

The Consortium of Multiple Sclerosis Centers has updated guidelines for using magnetic resonance imaging to evaluate people suspected of having multiple sclerosis. Doctors use the MRI guidelines not only to diagnose MS but also to track treatment results. A task force is reviewing the new guidelines before they're published. The working document is called  "Revised Guidelines of the CMSC MRI Protocol for the Diagnosis and Follow-up of MS." The task force, composed of neurologists, radiologists and imaging scientists experienced in MS, met in January 2017 to revise the guidelines. They also updated information about the situations for which standardized brain and spinal cord MRI scans should be used. One change is a recommendation that gadolinium, a contrast agent in scans, be used cautiously. The previous update, published in 2015, included no constraints on the use of gadolinium-based contrast agents. But soon after publication, information emerged showing that gadolinium, although not toxic, accumulates in the brain. This prompted the U.S. Food and Drug Administration to recommend limiting the use of gadolinium to “appropriate clinical circumstances.” To mirror the increased awareness of gadolinium deposits, the new guidelines say: “While there is no known central nervous system toxicity, these agents should be used judiciously, recognizing that gadolinium continues to play an invaluable role in specific circumstances related to the diagnosis and follow-up of individuals with MS.” Since 2009, the Consortium of Multiple Sclerosis Centers has addressed a number of other issues. One is encouraging the use of three-dimensional MRI for brain scans. Another is developing protocols for monitoring severe optic nerve inflammation and progressive multifocal leukoencephalopathy, or PML, a brain disease caused by a virus. The guidelines have been revised to recommend the specific timing of scans for monitoring PML. The update also includes recommendations for the timing of scans on patients receiving disease-modifying drugs. Since 2009, the guidelines have included recommendations on scans of radiologic isolated syndrome, a condition where MS-like MRI lesions are present without symptoms. And they have included provisions on the value of using MRI changes to evaluate treatment effectiveness. The centers' goal "is to standardize the MRI protocol and make these recommendations a useful guideline for neurologists, neuroradiologists, and related healthcare professionals during initial evaluations and during follow-up of patients with MS, and ultimately provide optimum care for those individuals dealing with this unpredictable disease,” June Halper, the centers' chief executive officer, said in a press release.

The 7th Joint ECTRIMS-ACTRIMS Meeting, taking place in Paris this month, is one of the largest scientific conferences focused solely on multiple sclerosis (MS), and the National Multiple Sclerosis Society will be among the many interested parties attending. To get a feeling for meeting highlights and presentations the…

The year’s largest gathering of multiple sclerosis “minds” starts on Oct. 25 in Paris. More than 8,000 neurologists, researchers and others who specialize in treating and curing MS will be attending MSParis2017. It’s a joint meeting of the European and the Americas Committee for Research in Multiple Sclerosis…

BC Platforms announced that Biogen and the Accelerated Cure Project (ACP) will use its platform to advance research in multiple sclerosis (MS) by bringing data collected through clinical trials, biobanks and the like directly to researchers and other experts in the field. Microsoft is also a project partner,…

Common Allergy Treatment Restores Protective Neuron Coating in MS, Trial Suggests This is the kind of news we all hope to hear. A treatment that will repair our frayed “wires” and, in doing so, restore some of the function that MS has stolen from us. This is…

Researchers found a significant increase in some types of gut bacteria and lower levels of an anti-inflammatory factor in untreated multiple sclerosis twins. The study offered working evidence that components of gut microbiota contribute to autoimmune diseases like MS. Researchers published their article in the journal Proceedings of the National Academy of Sciences.It was titled "Gut microbiota from multiple sclerosis patients enables spontaneous autoimmune encephalomyelitis in mice." Our gut contains millions of good bacteria, fungi, bacteria-like archaea, and viruses that we can't live without. Although there are 300 to 1,000 species of bacteria in our gut, most of our intestines is populated with 30 or 40 species. Recent increases in knowledge and technical advancements have made it possible for scientists to measure the equilibrium between different species in the gut, and analyze their influence on our health. One discovery was a link between the balance of bacteria in the intestines and autoimmune diseases like MS. A team of researchers decided to see if differences in gut microbiota play a role in MS progression and perhaps its onset. They analyzed the feces of 34 identical twins, one of each who had MS and one of each who didn't. They used twins to try to reduce genetic and environmental differences' influence on the onset of the disease. All of those with MS were Caucasian and had grown up with their healthy twin to adulthood. Researchers analyzed the type and abundance of microorganisms in the feces of both the MS-affected and healthy twins. They found no differences in species or amount of bacteria between siblings. What they did find was a significant increase in some types of bacteria, such as Akkermansia, in untreated twins with MS. The team transplanted fecal samples from MS-affected and healthy twins into a mice model of MS called experimental autoimmune encephalomyelitis. These animals have an inflammatory myelin-destroying disease of the central nervous system that is comparable to human MS. Myelin is a protective coating around neurons whose loss is associated with MS. MS twin-derived gut microbiota caused a significantly higher amount of mice to develop a relapsing–remitting autoimmunity similar to MS than healthy twin-derived microbiota. When researchers measured the microbial profiles of the mice's feces, they found significant differences in amounts of bacteria. The most important difference was in Sutterella, an organism that helps protect against inflammation. Sutturella levels were significantly reduced in the feces of mice transplanted with MS twin-derived microbiota compared with feces from healthy twins. The team also measured the mice's immune cells and the proteins they release. They discovered that immune cells in mice with MS-twin feces transplants produced less of the anti-inflammatory factor IL-10 than immune cells from mice colonized with healthy-twin samples. IL-10, or interleukin 10, is an important immune protein. When researchers transplanted the feces of healthy twins into the mice, then gave them an antibody that blocks the function of IL-10, they also became sick. This indicated that IL-10 may temper autoimmunity in the central nervous system. The team then measured the twins' immune blood components. They found that the healthy twin had higher quantities of IL-10 than the MS-affected one. This is a complex issue in which very subtle differences of type and amount of bacteria in the gut can have considerable consequences, they added.  

Aubagio (teriflunomide) may lead to reversible nail loss, researchers at Italy's University of Bologna reported after reviewing the case of a 55-year-old woman with relapsing-remitting multiple sclerosis. They described what happened to a patient who was referred to an MS clinic after experiencing acute optic neuritis — or inflammation of the optic nerve — three months earlier. Their report, “Nail loss after teriflunomide treatment: A new potential adverse event,” was published in the journal Multiple Sclerosis and Related Disorders. Doctors had been treating the woman with intravenous methylprednisolone. Physicians had judged her slightly disabled, with an Expanded Disability Status Scale (EDSS) score of 3, but had not diagnosed her with MS. When she was diagnosed a few months later, she began receiving interferon beta-1a. It did not work, so doctors switched her to Sanofi Genzyme's Aubagio. At first, she tolerated the treatment well, having only slight nausea after taking the medication. Physicians did not detect signs of liver toxicity or high blood pressure, which are relatively common side effects of Aubagio. Roughly three months after starting the medication, however, the woman began having more trouble walking problems and had mild hair loss. Two and a half months later, she said her nails had started falling out in the past month. When doctors examined her, she had lost two nails, while others appeared to have stopped growing. They were thinner than normal and some had detached from the nail bed. In addition, her hair loss continued. She had not started using other drugs, new cosmetics, or changed her diet. A dermatologist excluded the possibility that the condition was the result of fungus, psoriasis, or other conditions that could cause nails to fall off. Because doctors suspected that Aubagio could be the cause of the nail loss, they recommended that she stopped taking it. The patient switched to Biogen's Tecfidera (dimethyl fumarate) after a couple of weeks, and her nails started to grow again. This supported doctors’ idea that Aubagio had caused the nail loss, and that it was reversible. Nail growth is similar to that of hair, researchers said. The patient’s reaction could be an unusual version of the same process that makes people lose their hair when taking Aubagio, they said. Since nail loss is not described as a side effect of Aubagio on the medication's label, researchers urged MS specialists to consider the possibility if they see patients with the problem.  

Magnetic resonance imaging (MRI) brain scans of children could reveal changes associated with multiple sclerosis (MS) before any symptoms are developed, according to a study by scientists at Yale University School of Medicine. The findings suggest that brain and spinal cord scans can identify children at high risk for developing MS.

Scientists have been trying to find a way to restore a protective covering around nerve cells whose loss leads to the neuron damage associated with multiple sclerosis. A team at the University of California, San Francisco may have found a way to do it. And perhaps surprisingly, the possible solution…

A higher intake of dietary sodium, most often in the form of salt, does not increase the risk of developing multiple sclerosis (MS), Norwegian researchers concluded after analyzing data from more than 175,000 women. Their findings counter earlier evidence from experimental studies in cells and MS mouse models that suggested…

Diet can play an important role in whether children with relapsing multiple sclerosis have a relapse, researchers at the University of California, San Francisco argue. Their study demonstrated that a diet with a lot of fat increases the risk of a youngster having a relapse by 56 percent, with saturated fat tripling the risk. Eating a lot of vegetables, on the other hand, cuts the risk in half, the team said. Since children with MS tend to have relapses more often than adults, the researchers figured they would be a suitable group to study diet's impact on relapse. They recruited 219 children with relapsing-remitting MS or clinically isolated syndrome from 11 centers across the U.S. Clinically isolated syndrome is a condition that can evolve in MS. The research team use a questionnaire known as the Block Kids Food Screener to analyze what the youngsters ate. They tracked the children an average of almost two years, which was plenty of time for relapses to occur. And, in fact, they did occur in 42.5 percent of the group. It turned out that fat had a particularly devastating effect on the youngsters' relapse rate. For every 10 percent increase in energy intake that came from fat, there was a 56 percent increase in the children's risk of having a relapse. Saturated fats were the biggest driver of risk. When researchers look only at these fats, they discovered that the risk more than tripled. Examples of saturated fats include processed meats such as sausages, ham, and burgers, butter, hard cheeses, and whole milk. Vegetables had the opposite effect on risk, the researchers observed. Using a cup equivalent as a standardized measure, they learned that for every additional cup of vegetables the children ate, the risk of a relapse dropped in half. To exclude the possibility that other factors influenced the results, the team included information about age, sex, ethnicity, duration of disease, body mass index, treatment, and D-vitamin levels in their analyses. This did not influence the results. The team also looked at whether other food components, such as sugar, iron, fruit and fiber, would affect the risk of relapse. They did not find any links. Although the risk associations were strong, the researchers cautioned that the study's observational design meant that it was not able to prove that fat causes relapses. But there are several ways that fat could play a role in disease processes, they argued. For instance, high fat intake triggers the release of inflammation-promoting molecules. It also affectsf gut bacteria that are linked to immune processes. Vegetables lower the risk of inflammation and immune problems, the team said. In an accompanying editorial, Dr. Kathryn Fitzgerald of the Johns Hopkins School of Medicine said the study had important limitations. Researchers gathered information on the children's diet only in the week before they enrolled in the study. This might not adequately capture more long-term dietary patterns, she said. And fat is not simply fat, she pointed out, arguing that fish oil is believed to help MS patients. Although the California research offers insight, she called for long-term studies to define diet's role in MS.

Spain’s Oryzon Genomics will offer new data on the preclinical efficacy of ORY-2001, an epigenetic modulator it is developing to treat  multiple sclerosis (MS). Its presentation is set for Oct. 26 at MSParis2017, the joint international meeting of the European and Americas Committees for Treatment and Research in Multiple Sclerosis…

Pain, walking problems and fatigue are factors that most strongly lower self-perceived health in multiple sclerosis (MS), researchers at the New York University Langone Medical Center have found. This challenges current treatment approaches focus mainly on physical disability. It suggests that “invisible disability” may be more important to how patients…

The discovery of an immune cell quality control mission may have put scientists a step closer to understanding how autoimmune conditions such as multiple sclerosis arise. University of Alabama at Birmingham researchers identified regulatory immune cells with the quality control mission of destroying antibody-producing B-cells that mistakenly target the body's own tissue after an infection. An autoimmune disease is one in which the immune system attacks healthy tissue or organs instead of invaders. Eventually, the insight could lead researchers to new approaches for treating MS and other conditions caused by aberrant immune reactions. The Alabama researchers were studying the processes involved in the body's defense against a real threat — the influenza virus — when they discovered a population of immune cells whose action is relevant to autoimmune diseases. The study noted that T follicular regulatory cells appeared in the late stages of influenza infection. Their objective was to prevent the immune system from generating self-reactive antibodies — that is, those that attack the body's own tissue. These cells are poorly understood, the researchers explained. Their experiments, published in the journal Nature Immunology, focused on the molecular events surrounding the cells’ actions.  The team discovered that about a week after the infection, levels of an immune regulator called the IL-2 protein increased. This triggered the multiplication of common regulatory T-cells, or Tregs. When this phase of the immune reaction was fading, TFR cells started multiplying, reaching peak numbers about a month after infection. The formation of the TFR cells was therefore tightly linked to the processes controlling Treg production, researchers said, with falling levels of IL-2 allowing the new phase of the immune response. The TFR cells migrated to the lymph nodes — the headquarters of antibody-producing B-cells. Here, B-cells proliferate and change their antibody-producing genes to create new, stronger antibodies. But sometimes the gene changes, or mutations, give rise to an antibody that attacks the body, instead of invaders. Researchers discovered that TFR cells prevented B-cells, which gave rise to autoantibodies, from accumulating in the lymph nodes. Importantly, the TFR cells had no impact on the immune processes targeting the influenza virus. When researchers prevented TFR cells from forming or removed them from mice, the animals started producing autoantibodies, they explained. While this suggested that people with autoimmune diseases may have flawed TFR processes, the study did not investigate this, making the topic a possibility for future studies.

Nimbus Therapeutics and Celgene have agreed to work together to identify potential therapeutic compounds that can specifically target Tyk2 and STING — two proteins involved in inflammation and innate immune response. This strategic collaboration can open new therapeutic avenues for the treatment of multiple sclerosis (MS) and several autoimmune disorders. Nimbus, headquartered in Cambridge, Massachusetts, applies chemical computational analysis to identify and develop new compounds with potential for therapeutic use in a range of diseases. Two Nimbus immunology programs are already covered under the newly established agreement: one developing inhibitors of Tyk2 and antagonists of STING protein. Tyk2, or tyrosine kinase 2, mediates the signaling of several pro-inflammatory proteins, including interleukin (IL)-23, IL-12 and type-I interferons. Inhibiting this enzyme can stop signals from passing through. This can potentially impair inflammatory response. STING, or stimulator of interferon genes, is an important activator of immune responses. As such, finding ways to block its activity can help prevent autoimmunity and reestablish immune response balance. Under their accord, Nimbus will control the program's research and development; Celgene will have the option to acquire each program covered by the alliance.

Synthon’s prefilled syringe with 40 mg/ml of glatiramer acetate — the generic version of Teva Pharmaceutical’s Copaxone 40 mg — has received regulatory clearance in all 28 member states of the European Union (EU) plus Iceland, Liechtenstein and Norway to treat relapsing-remitting multiple sclerosis (RRMS). The low-dose…

Groundbreaking evidence of the existence of lymphatic vessels in the human brain could answer the question of how the brain gets rid of waste products, and holds clear implications for neuroinflammatory disorders such as multiple sclerosis. The lymphatic system is a network that helps the body to rid itself of toxins and waste products. Lymphatic vessels, which are similar to blood vessels, transport a clear fluid – lymph – which is filtered in lymph nodes. It has long been thought that the brain lacks lymphatic vessels. However, a team of researchers at the National Institutes of Health (NIH), building on previous research in rodent brains, recently found evidence that the brain may actually drain waste through lymphatic vessels. The researchers injected healthy volunteers with a magnetic dye called gadobutrol, which is usually used as a contrast agent to image blood vessels. They then scanned the brains of these individuals using magnetic resonance imaging (MRI) under specific settings. This allowed them to view the dye within the outer layer of the brain, known as the dura. The MRI revealed that the dye was visible both as dots and straight lines, which might indicate lymph vessels. This suggested that the dye leaked out of blood vessels into the dura and were later 'picked up' by lymphatic vessels. These vessels were not seen when the volunteers were injected with another dye that does not leak out of blood vessels. Evidence of lymphatic vessels in the brain was also found in autopsied human brain tissue. Although a pair of 2015 studies had shown evidence of lymphatic vessels in the brains of mice, this is the first study that demonstrates that a similar system exists in human brains. “For years we knew how fluid entered the brain. Now we may finally see that, like other organs in the body, brain fluid can drain out through the lymphatic system,” Reich said . In addition to changing the way we think about the lymphatic system and the brain, this study lays the foundations for future research to investigate whether the function of the lymphatic system is altered in the brains of patients with multiple sclerosis or other disorders affecting the nervous system.

Two short courses of Lemtrada prevented multiple sclerosis from becoming active and progressing for five years, a study reported. Lemtrada's maker, Sanofi-Genzyme, said the study covered the two-year CARE-MS II Phase 3 clinical trial (NCT00548405) and a long-term extension (NCT00930553) trial of people with relapsing-remitting MS. In addition to demonstrating Lemtrada's effectiveness, the study showed that it was safe, researchers said. The Phase 3 trial participants had had an active disease, with at least two relapses in the two years before the study and an inadequate response to earlier treatment. The trial compared Lemtrada's effectiveness with that of Rebif. The Lemtrada group received 12-mg doses for five consecutive days at the start of the study and three consecutive days a year later. Ninety-three percent of the 435 patients who completed the trial enrolled in the extension, which followed patients for another three years. Remarkably, 60 percent of patients required no additional treatment after the two years of the Phase 3 study. Among the 376 patients who required more treatment, 30 percent had one additional Lemtrada course, 10.4 percent had two, and 1.6 percent had three. A small proportion of patients also received other disease-modifying treatments. The most common reason for additional treatment was relapse. Nevertheless, Lemtrada reduced annualized relapse rates to only 0.18 of patients by the fifth year. In addition, during the five years, 75 percent of patients experienced no worsening of their disability over six-month cycles. And 49 percent of patients' disability improved. Researchers also tracked patients' scores on the NEDA — or No Evidence of Disease Activity — index. The composite measure takes into account relapses, disease activity detected in MRI scans, and disability progression. In year five, 58 percent of patients achieved NEDA, slightly more than the 53 percent in year three. Another important finding was that patients' loss of brain tissue slowed in the first two years, and dropped further during the extension. Researchers also noted that adverse events dropped during the extension trial. Ninety-six percent were mild or moderate, and no patient left the study because of side effects. The rate of infusion-associated reactions was lower in the extension study than in the Phase 3 study. Patients who did have a reaction most often experienced headache, fever, or rash. Infections did not become more common with accumulating Lemtrada doses and, again, were less common in the extension trial. Patients most often developed colds or urinary tract infections. Autoimmune reactions against the thyroid gland were relatively common, however. Thirty-eight percent of patients developed them over the five years. Most were moderate in severity. Four patients developed various types of cancers. Researchers also examined Lemtrada in the CARE-MS I clinical trial and its extension trial. They reported long-term outcomes and safety findings similar to those in the latest study. Overall, the newest results demonstrated that Lemtrada slowed disease progression over five years in relapsing-remitting MS patients who failed to respond to previous therapy.