Links for Keyword: Multiple Sclerosis

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By Carl Zimmer Multiple sclerosis, an autoimmune disease that affects 2.9 million people, presents a biological puzzle. Many researchers suspect that the disease is triggered by a virus, known as Epstein-Barr, which causes the immune system to attack the nerves and can leave patients struggling to walk or talk. But the virus can’t be the whole story, since nearly everyone is infected with it at some point in life. A new study found a possible solution to this paradox in the skeletal remains of a lost tribe of nomads who herded cattle across the steppes of western Asia 5,000 years ago. It turns out that the nomads carried genetic mutations that most likely protected them from pathogens carried by their animals, but that also made their immune systems more sensitive. These genes, the study suggests, made the nomads’ descendants prone to a runaway immune response. The finding is part of a larger, unprecedented effort to understand how the evolutionary past has shaped the health of living people. Researchers are analyzing thousands of genomes of people who lived between Portugal and Siberia and between Norway and Iran roughly 3,000 to 11,000 years ago. They hope to trace the genetic roots of not only multiple sclerosis, but also diabetes, schizophrenia and many other modern illnesses. “We are taking ancient human genomics to a whole new level,” said Eske Willerslev, a geneticist at the University of Copenhagen who led the effort. The researchers published the multiple sclerosis study as well as three other papers on the genetics and health of ancient peoples on Wednesday in the journal Nature. For more than a decade, Dr. Willerslev and other researchers have been pulling DNA from ancient human bones. By comparing the surviving genetic material with that of living people, the scientists have been able to track some of the most significant migrations of people across the world. © 2024 The New York Times Company

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 29093 - Posted: 01.11.2024

Nicola Davis Science correspondent Researchers have discovered a genetic variant that appears to influence the speed at which multiple sclerosis (MS) progresses, potentially paving the way for new treatments. According to the MS International Federation, about 2.9 million people worldwide have MS, a condition in which the insulating coating of the nerves in the brain and spinal cord is damaged by the immune system. The nerve fibres themselves can also become damaged. While some people have a relapsing remitting form of the disease, others experience gradual progression that in some can cause severe disability. Researchers say they have identified a genetic variant that appears to increase the severity of the disease. They found that people who inherit the variant from both parents need a walking aid almost four years sooner than those without. “This is a very substantial effect for a single genetic variant,” said Sergio Baranzini, a professor of neurology at the University of California, San Francisco and co-senior author of the study. “Furthermore, this variant affects genes that are active in the central nervous system, a clear contrast to variants that confer risk [of MS], which overwhelmingly affect the immune system.” The study, published in the journal Nature, was an international endeavour, involving 70 institutions around the world. To make their discovery, the team analysed genetic data from more than 12,000 people with MS, screening more than 7m genetic variants for associations with the speed of disease progression. The team found that one variant, nestled between two genes called DYSF and ZNF638, was associated with a more rapid increase in disability. © 2023 Guardian News & Media Limited

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28840 - Posted: 07.01.2023

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 28565 - Posted: 11.23.2022

By Erin Garcia de Jesús As Tanina Agosto went through her normal morning routine in July 2007, she realized something was wrong. The 29-year-old couldn’t control her left side, even her face. “Literally the top of my head to the bottom of my foot on the left side of my body could not feel anything.” The next day, Agosto spoke with a doctor at the New York City hospital where she works as a medical secretary. He told her that she probably had a pinched nerve and to see a chiropractor. But chiropractic care didn’t help. Months later, Agosto needed a cane to get around, and moving her left leg and arm required lots of concentration. She couldn’t work. Numbness and tingling made cooking and cleaning difficult. It felt a bit like looping a rubber band tightly around a finger until it loses sensation, Agosto says. Once the rubber band comes off, the finger tingles for a bit. But for her, the tingling wouldn’t stop. Finally, she recalls, one chiropractor told her, “I’m not too big of a person to say there’s something very wrong with you, and I don’t know what it is. You need to see a neurologist.” In November 2008, tests confirmed that Agosto had multiple sclerosis. Her immune system was attacking her brain and spinal cord. Agosto knew nothing about MS except that a friend of her mother’s had it. “At the time, I was like, there’s no way I’ve got this old lady’s condition,” she says. “To be hit with that and know that there’s no cure — that was just devastating.” Why people develop the autoimmune disorder has been a long-standing question. Studies have pointed to certain gene variations and environmental factors. For decades, a common virus called Epstein-Barr virus has also been high on the list of culprits. © Society for Science & the Public 2000–2022.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28428 - Posted: 08.11.2022

By Kim Tingley Denis Burkitt, an Irish surgeon, traveled to Africa during World War II as a member of the Royal Army Medical Corps, and afterward he settled in Uganda to practice medicine. There he observed that a surprising number of children developed strange jaw tumors, a cancer that would come to be known as Burkitt lymphoma. Eventually, Burkitt sent samples of the tumor cells to Middlesex Hospital Medical School in London, where Michael Anthony Epstein, a pathologist, and his colleagues Yvonne Barr and Bert Achong examined them through an electron microscope. Their findings — they noticed particles shaped like a herpesvirus, only smaller — were published in a landmark paper in The Lancet in 1964 and spurred the realization that this newly identified member of the Herpes​viridae family, subsequently named Epstein-Barr virus, was a cause of Burkitt lymphoma. It was the first evidence that a viral infection could lead to cancer. The virus has since been shown to increase the risk of Hodgkin lymphoma, as well as nasopharyngeal and stomach cancer. It is also the virus most often responsible for infectious mononucleosis, a disease usually characterized by extreme fatigue, sore throat, fever and swollen lymph nodes in the neck. These symptoms can last for weeks and, in chronic cases, recur for years. We now know that upward of 90 percent of adults have the Epstein-Barr virus. As happens with other herpes​viruses, once you have been infected, the virus stays with you forever — it deposits its DNA alongside yours in the nucleus of many of your cells. (RNA viruses, like SARS-CoV-2, can be cleared from your body.) Most people contract Epstein-Barr in childhood: It is spread through body fluids, usually saliva; kissing is a frequent route of transmission (as may be the sharing of utensils). Young children, if they get sick at all, typically develop symptoms indistinguishable from those of a cold or flu; mono is more common when the first infection happens after puberty. “Most people never know they’re infected,” says Jeffrey Cohen, the chief of the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases. © 2022 The New York Times Company

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28223 - Posted: 02.26.2022

By Gina Kolata For decades, researchers have suspected that people infected with an exceedingly common virus, Epstein-Barr, might be more likely to develop multiple sclerosis, a neurological illness that affects a million people in the United States. Now, a team of researchers reports what some say is the most compelling evidence yet of a strong link between the two diseases. The virus infects nearly everyone in their teen or young adult years, and very few go on to develop multiple sclerosis. The researchers also note that it is not the only known risk factor for people who develop the illness. But they say their data points to it being the clearest of them all. While it remains to be seen whether the finding will result in treatments or cures for multiple sclerosis, the study may further motivate research into therapies and vaccines for the condition. In their study, published Thursday in Science, the group examined data from 10 million people on active duty in the United States Armed Forces over two decades. The strength of their study, said its principal investigator, Dr. Alberto Ascherio, an epidemiologist at the Harvard T.H. Chan School of Public Health, is that they were able to follow people for years and ask whether infections with Epstein-Barr preceded multiple sclerosis. Among the service members in the study, 801 developed multiple sclerosis, a disabling disease that occurs when the immune system attacks the fatty insulation that protects nerves in the brain and spinal cord. Most who develop the disease are diagnosed between the ages of 20 and 50. The disease is rare, though — an individual’s chance of getting multiple sclerosis is half of one percent. At the same time, the virus in question, Epstein-Barr, is common, infecting nearly everyone in the population at some point. Although few are aware that they were infected, some develop mononucleosis. The virus remains in the body for life. © 2022 The New York Times Company

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28154 - Posted: 01.15.2022

By Dave Itzkoff Selma Blair could only talk for a half-hour in our first session. That was as long as she trusted her brain and her body to cooperate — any longer and she feared that her focus might start to wander or her speech might begin to trail. “We’re being responsible in knowing that smaller moments will be clearer moments,” she said. For Blair no day is free from the effects of multiple sclerosis, the autoimmune disease that she learned she had in 2018 but that she believes began attacking her central nervous system many years earlier. This particular Friday in September had started out especially tough: She said she woke up in her Los Angeles home feeling “just bad as all get out,” but she found that talking with people helped alleviate her discomfort. Blair said she had had good conversations earlier in the day and that she had been looking forward to ours. So, if she needed to take a break during this interview, she said with a delighted cackle, “it just means you’re boring me.” An unparalleled lack of inhibition has always defined Blair’s best-known work. She is 49 now, with a résumé that includes seminal works of teensploitation (“Cruel Intentions”), comedy (“Legally Blonde”) and comic-book adventure (“Hellboy”). ImageBlair in one of her signature roles, as a fellow law student opposite Reese Witherspoon in “Legally Blonde.” That same unbridled bluntness persists in all her interactions, whether scripted or spontaneous, with cameras on or off, even when she is sharing her account of the time she went on “The Tonight Show” wearing a strappy top she accidentally put on sideways. It is a story she told me proudly, within five minutes of our introduction on a video call, while her fingers made a maelstrom of her close-cropped, bleached-blond hair. (By way of explaining this style choice, she burst into a brassy, Ethel Merman-esque voice and sang, “I want to be a shiksa.”) But Blair’s candor has come to mean something more in the three years since she went public about her M.S. diagnosis. Now, whether she is posting personal diaries on social media or appearing on a red carpet, she understands she is a representative with an opportunity to educate a wider audience about what she and others with M.S. are experiencing. © 2021 The New York Times Company

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 28030 - Posted: 10.13.2021

Ian Sample Science editor Doctors believe they are closer to a treatment for multiple sclerosis after discovering a drug that repairs the coatings around nerves that are damaged by the disease. A clinical trial of the cancer drug bexarotene showed that it repaired the protective myelin sheaths that MS destroys. The loss of myelin causes a range of neurological problems including balance, vision and muscle disorders, and ultimately, disability. While bexarotene cannot be used as a treatment, because the side-effects are too serious, doctors behind the trial said the results showed “remyelination” was possible in humans, suggesting other drugs or drug combinations will halt MS. Advertisement “It’s disappointing that this is not the drug we’ll use, but it’s exciting that repair is achievable and it gives us great hope for another trial we hope to start this year,” said Prof Alasdair Coles, who led the research at the University of Cambridge. MS arises when the immune system mistakenly attacks the fatty myelin coating that wraps around nerves in the brain and spinal cord. Without the lipid-rich substance, signals travel more slowly along nerves, are disrupted, or fail to get through at all. About 100,000 people in the UK live with the condition. Funded by the MS Society, bexarotene was assessed in a phase 2a trial that used brain scans to monitor changes to damaged neurons in patients with relapsing MS. This is an early stage of the condition that precedes secondary progressive disease, where neurons die off and cause permanent disability. © 2020 Guardian News & Media Limited

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27496 - Posted: 09.28.2020

Sydney Lupkin Sometimes, the approval of a new generic drug offers more hype than hope for patients' wallets, as people with multiple sclerosis know all too well. New research shows just how little the introduction of a generic version of Copaxone — one of the most popular MS drugs — did to lower their medicine costs. MS is an autoimmune disease that gradually damages the central nervous system, disrupting communication between the brain and the rest of the body. Its symptoms are different from patient to patient across a lifetime but can include weakness, numbness, vision problems, tremors and even paralysis. There's no cure for MS, though some patients experience long remissions of symptoms. Several prescription drugs can stave off multiple sclerosis attacks and slow down the disease, says Deborah Ewing-Wilson, a neurologist with University Hospitals Cleveland Medical Center. But the cost of some of the most effective medicines — which have undergone frequent price hikes over the years — can put added stress on her patients. "They are extremely expensive," says Ewing-Wilson. On average, the medicines cost $70,000 per year, according to a 2017 study. Some prices have increased fivefold from when the drugs were first approved by the Food and Drug Administration. Even with insurance, says Ewing-Wilson, patients can be left on the hook for anywhere from $3,000 to more than $50,000 a year. Some patients tell her they need to skip their medications altogether because they're unaffordable. So when a generic version of the injectable MS drug Copaxone — also known as glatiramer acetate — was launched in 2015, Dan Hartung, a drug policy researcher at Oregon Health & Science University, and his colleagues thought that might spur some price relief. After all, if a cheap multiple sclerosis drug were available, wouldn't patients flock to it, forcing other manufacturers to lower their prices to compete? © 2020 npr

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26980 - Posted: 01.22.2020

Katarina Zimmer As early as the 1990s, researchers proposed that a very common type of herpes virus—then known as human herpesvirus 6 (HHV6)—could be somehow involved in the development of multiple sclerosis, a neurodegenerative disease characterized by autoimmune reactions against the protective myelin coating of the central nervous system. However, the association between HHV6 and the disease soon became fraught with controversy as further studies produced discordant results. Complicating matters further, HHV6 turned out to be two related, but distinct variants—HHV6A and HHV6B. Because the two viruses are similar, for a while no method existed to tell whether a patient had been infected with one or the other, or both—making it difficult to draw a definitive association between either of the viruses and the disease. Now, a collaboration of European researchers has developed a technique capable of distinguishing antibodies against one variant from the other. Using that method in a Swedish cohort of more than 8,700 multiple sclerosis patients and more than 7,200 controls, they found that patients were much more likely to carry higher levels of anti-HHV6A antibodies than healthy people, while they were likelier to carry fewer antibodies against HHV6B. The findings, published last November in Frontiers in Immunology, hint that previous contradictory results may at least be partially explained by the fact that researchers couldn’t distinguish between the two viruses. “This article now makes a pretty convincing case that it is HHV6A that correlates with multiple sclerosis, and not HHV6B,” remarks Margot Mayer-Pröschel, a neuroscientist at the University of Rochester Medical Center who wasn’t involved in the study. “Researchers can now focus on one of these viruses rather than looking at [both] of them together.” © 1986–2020 The Scientist.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26956 - Posted: 01.14.2020

By Sofie Bates In multiple sclerosis, barriers that guard the brain become leaky, allowing some disease-causing immune cells to invade. Now scientists have identified a key molecule in the process that helps B cells breach the barriers. ALCAM, a protein produced by B cells, helps the immune cells sneak into the central nervous system, researchers report November 13 in Science Translational Medicine. Tests in mice and in artificial human brain barriers show that B cells without ALCAM, or activated leukocyte cell adhesion molecule, had trouble getting through the brain’s barriers. And in mice with a disease with some characteristics similar to MS, blocking ALCAM seemed to alleviate the disease’s severity. These early results indicate that the protein may be a good target for new treatments for multiple sclerosis in people, the researchers say. “This is a very important puzzle piece in how we understand multiple sclerosis,” says David Leppert, a neurologist at the University Hospital Basel in Switzerland who was not involved in the work. “How it translates into clinical applications is yet another question.” Worldwide, over 2.3 million people have multiple sclerosis, including nearly 1 million adults in the United States. Scientists think that rogue immune cells invade the brain and strip away the protective coating on nerve cells — leading to neurological issues and physical disability as the disease progresses. There’s no cure, and treatments don’t work for advanced stages of multiple sclerosis. Scientists have developed over a dozen medications to treat MS symptoms (SN: 11/29/17), one of which uses antibodies to destroy the body’s B cells. But that approach weakens patients’ immune systems, opening the door for future infections or cancer. In the new study, the researchers are instead focusing on preventing disease-causing B cells from entering the brain. © Society for Science & the Public 2000–2019

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26859 - Posted: 11.29.2019

Ashley P. Taylor Autoimmune diseases tend to ease up during pregnancy, and for women with multiple sclerosis, physicians have documented fewer relapses of the condition while women are pregnant compared to before and after having a baby. Anecdotally, many MS patients also feel better when they’re expecting. Researchers believe that this happens because during pregnancy, the body reins in its immune response so as to not reject the fetus—and in doing so counteracts autoimmune diseases. But as to how exactly this all works, scientists are uncertain. “Obviously, everybody would love to understand why it happens because if you could bottle that property of pregnancy, perhaps you could use it therapeutically,” Adrian Erlebacher, a reproductive immunologist at the University of California, San Francisco, tells The Scientist. To investigate why this happens in pregnant women with multiple sclerosis (MS), Stefan Gold, a neuroscientist at the Institute of Neuroimmunology and Multiple Sclerosis at the Universitätsklinikum Hamburg-Eppendorf, in Hamburg, Germany, and colleagues examined T cell populations in 11 MS patients before, during, and after pregnancy and in 12 women without MS during and after pregnancy. They categorized the T cells into different groups based on a genetic analysis of the cells’ receptors. In the first trimester, they found, MS patients’ T cells were dominated by just a few types, called clones, each with a different T cell receptor. Between the first and third trimesters, those dominant clones declined in abundance, and T cells became more evenly distributed across the different populations, Gold says. In women without MS, the pregnancy-associated changes in the T cell repertoire were not significant. Gold and his colleagues reported their results in Cell Reports on October 22. © 1986–2019 The Scientist.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26830 - Posted: 11.19.2019

By Caroline Wyatt BBC News "I don't like to think of the future. It's such a big question mark. I just keep living in the present." Karine Mather was diagnosed with MS when she was 27, although she noticed the first symptoms much earlier. It started off as a mental-health issue with anxiety and depression, she remembers. Later, she noticed she was starting to limp when she walked longer distances. Karine began using a walker to help with her balance and stamina, and then a scooter when she could no longer walk very far. "I got to the stage where the wheelchair became quite liberating, and gave me back a sense of freedom again. Now I rely on the power-chair full-time because I can't stand by myself any more." Now Karine and her wife, Sarah, have had to give up their full-time jobs. Karine was forced to stop working as a customer service adviser at a bank because she could no longer fulfil the physical demands of work and Sarah gave up working as a data analyst so she could take care of Karine. Now 34, Karine retains the use of just one hand, and suffers pain, stiffness and spasticity in her body that has got worse as the disease has progressed. "It feels like a fist clenching all the time. And I have days when my mind is cloudy and I miss out words and sentences." Both remain upbeat but the financial, as well as the emotional, impact of MS has been huge. Karine's MS is the type known as "primary progressive", or PPMS, which meant that for the first years after diagnosis, no disease-modifying treatment was available. One new drug - Ocrevus, or ocrelizumab - was recently licensed for early PPMS in the UK but came too late to help Karine. Now the MS Society is launching an ambitious "Stop MS" appeal, aiming to raise £100m to fund research over the next decade into treatments that can stop the progression of disability in MS. © 2019 BBC

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26682 - Posted: 10.09.2019

Bret Stetka As the story goes, nearly 80 years ago on the Faroe Islands - a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore. Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not, zero, according to the tantalizing lore I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers. We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is. But infection does likely play a role in MS. As may be the case in Alzheimer's disease, it's looking more and more like MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS, and perhaps prevent it in the first place. In the MS-free brain, electrical impulses zip down nerve fibers called axons causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement. In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel. © 2019 npr

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25893 - Posted: 01.22.2019

By Kelly Servick In multiple sclerosis (MS), a disease that strips away the sheaths that insulate nerve cells, the body’s immune cells come to see the nervous system as an enemy. Some drugs try to slow the disease by keeping immune cells in check, or by keeping them away from the brain. But for decades, some researchers have been exploring an alternative: wiping out those immune cells and starting over. The approach, called hematopoietic stem cell transplantation (HSCT), has long been part of certain cancer treatments. A round of chemotherapy knocks out the immune system and an infusion of stem cells—either from a patient’s own blood or, in some cases, that of a donor—rebuilds it. The procedure is already in use for MS and other autoimmune diseases at several clinical centers around the world, but it has serious risks and is far from routine. Now, new results from a randomized clinical trial suggest it can be more effective than some currently approved MS drugs. “A side-by-side comparison of this magnitude had never been done,” says Paolo Muraro, a neurologist at Imperial College London who has also studied HSCT for MS. “It illustrates really the power of this treatment—the level of efficacy—in a way that’s very eloquent.” Nearly 30 years ago, when hematologist Richard Burt saw how HSCT worked in patients with leukemia and lymphoma, he was struck by a curious effect: After those patients rebuilt their immune systems, their childhood vaccines no longer protected them, recalls Burt, now at Northwestern University’s Feinberg School of Medicine in Evanston, Illinois. Without a new vaccination, the new immune cells wouldn’t recognize viruses such as measles and mumps and launch a prompt counterattack. That suggested that in the case of an autoimmune disease, reseeding the immune system might help the body “forget” that its own cells were the enemy. © 2018 American Association for the Advancement of Science

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 25870 - Posted: 01.16.2019

By Mitch Leslie Our immune cells normally pounce on intruding bacteria and viruses. But in multiple sclerosis (MS), immune cells target the nervous system instead. Now, researchers may have pinpointed a long-sought molecule called a self-antigen that provokes these attacks, pointing a way toward potential new treatments. “The work is monumental, and it’s tantalizing,” says neuroimmunologist Hartmut Wekerle of the Max Planck Institute of Neurobiology in Munich, Germany, who wasn’t connected to the research. Researchers have long suspected that a self-antigen—a normal molecule in the body that the immune system mistakenly treats as a threat—can trigger MS. The prime suspects have been proteins in myelin, the nerve insulation that erodes in patients with the disease. But after years of searching, scientists haven’t been able to pinpoint the molecule. To uncover other candidates, immunologists Roland Martin and Mireia Sospedra of University Hospital of Zurich in Switzerland and their colleagues analyzed immune cells known as T cells that came from a patient who died from MS. T cells normally switch on when they encounter protein fragments containing just a few amino acids that belong to an invading microbe, but they also turn on in people who have MS. The researchers wanted to determine which protein shards stimulated the patients’ T cells, so they tested 200 fragment mixtures, each containing 300 billion varieties. The two fragments with the strongest effect turned out to be part of a human enzyme called guanosine diphosphate-L-fucose synthase, which helps cells remodel sugars that are involved in everything from laying down memories to determining our blood type. T cells from 12 of 31 patients who had who either had been diagnosed with MS or had shown early symptoms of the disease also reacted to the enzyme, the researchers report online today in Science Translational Medicine. What’s more, T cells from four of the eight patients tested responded to a bacterial version of the enzyme—lending credence to the recently proposed idea that intestinal bacteria may help spark the disease. © 2018 American Association for the Advancement of Science

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25560 - Posted: 10.11.2018

Results from a clinical trial of more than 250 participants with progressive multiple sclerosis (MS) revealed that ibudilast was better than a placebo in slowing down brain shrinkage. The study also showed that the main side effects of ibudilast were gastrointestinal and headaches. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and published in the New England Journal of Medicine. “These findings provide a glimmer of hope for people with a form of multiple sclerosis that causes long-term disability but does not have many treatment options,” said Walter J. Koroshetz, M.D., director of the NINDS. Robert J. Fox, M.D., a neurologist at Cleveland Clinic in Ohio, led a team of researchers across 28 clinical sites in a brain imaging study to investigate whether ibudilast was better than placebo in reducing the progression of brain atrophy, or shrinkage, in patients with progressive multiple sclerosis. In the study, 255 patients were randomized to take up to 10 capsules of ibudilast or placebo per day for 96 weeks. Every six months, the participants underwent MRI brain scans. Dr. Fox’s team applied a variety of analysis techniques on the MRI images to assess differences in brain changes between the two groups. The study showed that ibudilast slowed down the rate of brain atrophy compared to placebo. Dr. Fox and his colleagues discovered that there was a difference in brain shrinkage of 0.0009 units of atrophy per year between the two groups, which translates to approximately 2.5 milliliters of brain tissue. In other words, although both groups experienced atrophy, the brains of the patients in the placebo group shrank on average 2.5 milliliters more over two years compared to the ibudilast group. The whole adult human brain has a volume of approximately 1,350 milliliters. However, it is unknown whether that difference had an effect on symptoms or loss of function.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25400 - Posted: 08.31.2018

By Abby Olena The gut-brain axis is line of communication between the two organs, involved in everything from brain development to the progression of neurological diseases, with gut microbiota often pitching in to the conversation. In a study published today (May 16) in Nature, researchers present evidence that multiple sclerosis (MS) may also be influenced by commensal microbes in the gut acting upon cells in the brain. They show in a mouse model of the disease that metabolites from gut bacteria alter the behavior of microglia—immune cells that reside in the brain—which in turn regulate the activity of astrocytes to promote or prevent inflammation. The authors also found evidence in vitro and in patient samples that a similar gut-brain connection exists in people with MS, suggesting that microbes and the cells that receive their signals could be targets for disease treatment. “The beauty of this paper is that it provides a very detailed mechanistic understanding of how things work,” Jonathan Kipnis, a neuroscientist at the University of Virginia who did not participate in the study, tells The Scientist. Previous research linked the microbiome and the development of MS in mice, he says, but “we never understood how the gut communicates with the brain.” In work published in Nature Medicine in 2016, Francisco Quintana of Brigham and Women’s Hospital in Boston and colleagues found part of the answer to the question of gut-brain communication. In that study, they showed that mouse and human astrocytes—star-shape glial cells—respond to molecules generated by microbes from the intestine. And because prior work from other groups had demonstrated that microglia can regulate astrocyte behavior, Quintana says, “one of the biggest unanswered questions we had is: what mediates the crosstalk between microglia and astrocytes?” © 1986-2018 The Scientist

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24992 - Posted: 05.18.2018

Fergus Walsh Doctors say a stem cell transplant could be a "game changer" for many patients with multiple sclerosis. Results from an international trial show that it was able to stop the disease and improve symptoms. It involves wiping out a patient's immune system using cancer drugs and then rebooting it with a stem cell transplant. Louise Willetts, 36, from Rotherham, is now symptom-free and told me: "It feels like a miracle." A total of 100,000 people in the UK have MS, which attacks nerves in the brain and spinal cord. Just over 100 patients took part in the trial, in hospitals in Chicago, Sheffield, Uppsala in Sweden and Sao Paolo in Brazil. They all had relapsing remitting MS - where attacks or relapses are followed by periods of remission. The interim results were released at the annual meeting of the European Society for Bone and Marrow Transplantation in Lisbon. The patients received either haematopoietic stem cell transplantation (HSCT) or drug treatment. After one year, only one relapse occurred among the stem cell group compared with 39 in the drug group. After an average follow-up of three years, the transplants had failed in three out of 52 patients (6%), compared with 30 of 50 (60%) in the control group. Those in the transplant group experienced a reduction in disability, whereas symptoms worsened in the drug group. Prof Richard Burt, lead investigator, Northwestern University Chicago, told me: "The data is stunningly in favour of transplant against the best available drugs - the neurological community has been sceptical about this treatment, but these results will change that. Prof John Snowden, director of blood and bone marrow transplantation at Sheffield's Royal Hallamshire Hospital, told me: "We are thrilled with the results - they are a game changer for patients with drug resistant and disabling multiple sclerosis". © 2018 BBC

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24767 - Posted: 03.19.2018

Children and adults who spend a lot of time outside in the summer may be less likely to develop multiple sclerosis years later, a U.S. study suggests. Sun exposure is thought to lessen the risk of MS, a chronic disease in which a person's immune system targets nerve cells in the brain and spinal cord, leading to damage. It is estimated Canada may have among the highest prevalence of MS in the world. While the disease is common, little is known about its causes. But for more than 10 years, sun exposure has been thought to be linked to MS risk. Previously, researchers focused on how UV-B rays from sunlight seem protective during childhood years. Now, University of British Columbia neurology professor Helen Tremlett and her co-authors have taken a broader view, extending the association into adulthood. In Wednesday's online issue of the journal Neurology, Tremlett and her team report combing through data on 151 women with MS and 235 others of similar age without the disease who were all participating in the Nurses' Health Study based in Boston. The long-running U.S. study is one of the largest investigations into risk factors such as diet, hormones, and environment for major chronic diseases in women. "We found that just generally going out in the summer was a beneficial thing and didn't matter so much if you were exposing yourself to direct sunlight. It was just going out in the summer that was associated with a reduced risk," Tremlett said in an interview. ©2018 CBC/Radio-Canada.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 10: Biological Rhythms and Sleep
Link ID: 24731 - Posted: 03.08.2018