Links for Keyword: Multiple Sclerosis

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Dr. Luanne Metz, an associate professor of neurosciences and physician-scientist in the Neuroscience Research Group at the University of Calgary’s Faculty of Medicine, has found that minocycline, a drug currently used to treat such conditions as acne, decreases the activity of lesions in the brains of people suffering from multiple sclerosis (MS). The results of her study are published in the May edition of the Annals of Neurology. The randomized study looks at ten people with active relapsing-remitting MS - characterized by clearly defined attacks (relapses) followed by partial or complete recovery (remissions). It assesses the effect of oral minocycline on people with active lesions in their brains. Each participant was given an MRI at the onset of the study, and then every four weeks after that, to determine whether or not the lesions caused by MS were getting worse or stabilizing. "For reasons that are still unclear, people with MS suffer from immune system malfunctions which trigger attacks of the nerve cells and myelin in the central nervous system,” says Metz, Director of the Calgary Health Region’s world renowned MS Clinic. “Current treatments being used today do not eliminate MS completely – they only lessen the severity and slow progression of the disease. Our new findings are exciting because we discovered that minocycline significantly reduces the activity of the lesions in the brain. These findings offer us the possibility of a new and safe treatment option for people with MS.”

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 5584 - Posted: 06.24.2010

ST. PAUL, MN – Women who take vitamin D supplements through multivitamins are 40 percent less likely to develop multiple sclerosis (MS) than women who do not take supplements, according to a study published in the January 13 issue of Neurology, the scientific journal of the American Academy of Neurology. Food is a source of vitamin D, and the body makes vitamin D through exposure to sunlight. "Because the number of cases of MS increases the farther you get from the equator, one hypothesis has been that sunlight exposure and high levels of vitamin D may reduce the risk of MS," said study author Kassandra Munger, MSc, of Harvard School of Public Health in Boston, MA. "This is the first prospective study to look at this question. "These results need to be confirmed with additional research, but it's exciting to think that something as simple as taking a multivitamin could reduce your risk of developing MS."

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 4795 - Posted: 06.24.2010

ST. PAUL, MN – Smokers are nearly twice as likely to develop multiple sclerosis (MS) as people who have never smoked, according to a study published in the October 28 issue of Neurology, the scientific journal of the American Academy of Neurology. The risk was increased for people whether they were smokers at the time they developed MS or were past smokers. "This is one more reason for young people to avoid smoking," said study author Trond Riise, PhD, of the University of Bergen in Norway. "Hopefully, these results will help us learn more about what causes MS by looking at how smoking affects the onset of the disease."

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 4430 - Posted: 06.24.2010

ST. PAUL, MN – Using MRI scans can help make the diagnosis of multiple sclerosis (MS) more quickly, according to a guideline developed by the American Academy of Neurology. The guideline is published in the September 9 issue of Neurology, the scientific journal of the American Academy of Neurology. The point at which MS can be diagnosed has been under debate, according to guideline author Elliot Frohman, MD, PhD, of the University of Texas Southwestern Medical School in Dallas. “Before, the criteria used to diagnose people required neurologists to show that disease activity had occurred in the brain over time,” said Frohman. “People would have to wait for a diagnosis. Now that we have evidence showing that early treatment can reduce the entire course of the disease, we really needed to ask the question about how early the diagnosis can be made.”

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 4263 - Posted: 06.24.2010

Montreal, . A new discovery by scientists at the Montreal Neurological Institute at McGill University may provide insights into Multiple Sclerosis. In a study published in the May issue of the Journal of Neuroscience (J. Neuroscience 2003 23: 3735-3744), Dr. Tim Kennedy and colleagues have discovered that a protein called netrin-1 directs the normal movement of the cells that become oligodendrocytes in the developing spinal cord. Oligodendrocytes are the cells that provide critical support for the nerve cells – they make myelin, the electrical insulation of the central nervous system. They are also the cells that degenerate and die in Multiple Sclerosis (MS). Although oligodendrocytes play an essential role in the nervous system, many aspects of their basic cell biology are not well understood, which is one of the reasons why MS is such a mystery. This research finding identifies a fundamental mechanism that directs migrating oligodendrocyte precursor cells. This has implications for understanding demyelinating diseases such as MS, where even a small myelin deficit can lead to functional impairment of the nerve cell. An estimated 50,000 people have MS, which is most often diagnosed in young adults. Its devastating effects last a lifetime and may include problems in seeing or speaking, difficulty with balance and coordination, and even paralysis. “Dr. Kennedy's research will contribute to the growing body of knowledge which is developing new therapies for MS," said Dr. William McIlroy, MS Society of Canada national medical advisor.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 3796 - Posted: 06.24.2010

In multiple sclerosis, new drugs and new insights are giving rise to new hopes BY KATHERINE HOBSON Lawrence Vail knew something was terribly wrong. More than a year ago, he was walking across a busy street in Boston when his leg went numb. Then came double vision and a mental fog that was so bad the 44-year-old thought he'd have to quit his job. But almost as quickly as he was diagnosed with multiple sclerosis, his doctor at Boston's Brigham and Women's Hospital put him on Avonex, one of several MS drugs approved over the past decade. After the disease changed his life, the medicine has changed it back. He can talk and express himself again. "The drug meant you go from the edge of the cliff to about 30 feet before the edge," he says. Tanya Pugliano, another MS patient at Brigham, also tried Avonex. But it didn't stop her legs from giving out or her hands from going numb. Neither did another MS drug, Copaxone. Now the 29-year-old is undergoing monthly chemotherapy treatments, like a cancer patient, trying yet another way of fighting back against the disease. Had either patient developed MS 15 years ago, even doctors at renowned medical centers like Brigham would have had little to offer them. They would have been powerless to stop the basic disaster of MS: a patient's immune system that savagely assaults the nerves in the brain and spinal cord. Now, thanks to a handful of recently developed drugs–one just approved a few months ago–physicians can blunt this attack. "It's not a cure, but it's a far cry from what we had before," says neurologist Fred Lublin, director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at Mount Sinai Hospital in New York. Copyright © 2002 U.S. News & World Report, L.P.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 2747 - Posted: 06.24.2010

ST. PAUL, MN – Researchers analyzing the records of 1,378 patients from three clinical trials of mitoxantrone as a treatment for multiple sclerosis (MS) reveal a small, but significant risk for developing diminished left ventricular ejection fraction (LVEF), which is a decrease in function of the left ventrical, and a lesser risk for congestive heart failure following treatment. The study is reported in the latest issue of Neurology, the scientific journal of the American Academy of Neurology. Mitoxantrone (MITO) is approved in the United States for the treatment of worsening relapsing-remitting, secondary-progressive, and progressive-relapsing MS. Unlike patients with leukemia and solid tumors who most often receive MITO in combination with other drugs, patients with MS are treated with MITO as a single drug to alleviate disease symptoms, said study author Donald Goodkin, MD, medical affairs director with Amgen Corp., a U.S. marketer of mitoxantrone in the United States. Cardiac toxicity, which may cause tachycardia and arrhythmia, LVEF, or congestive heart failure, has already been observed and reported in cancer patients who receive mitoxantrone as a chemotherapeutic agent.

Related chapters from BP7e: Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 2728 - Posted: 06.24.2010

DALLAS – A common drug given to multiple sclerosis patients appears to stimulate weakened immune system cells, according to a study published by researchers at UT Southwestern Medical Center at Dallas. While Copaxone, or glatiramer acetate, has long been known to slow or stop the progression of attacks in MS patients, researchers have not known exactly how the drug treated the disease. In the March issue of the Journal of Clinical Investigation, lead author Dr. Nitin Karandikar, UT Southwestern assistant professor of pathology and neurology, and colleagues report that Copaxone appears to stimulate a certain type of T cell in MS patients. Produced by the thymus gland, T cells are white blood cells that fight infection and, in healthy people, coordinate the body’s immune response. There are two types of T cells, CD4 and CD8 cells. Both are involved in the immune process that underlies MS and, in MS patients, the cells function abnormally to give rise to this disease. The researchers used flow cytometry to analyze cells taken from MS patients and were able to see the T cells rallying under the effect of Copaxone.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 1760 - Posted: 06.24.2010

By Brandon Keim The most detailed genetic investigation ever of multiple sclerosis has produced more questions than answers. Using extremely fine-grained analytical tools, scientists compared genetic information in three sets of identical twins. One of each pair had MS, and the other didn’t — yet their genes proved essentially identical. “We find no smoking gun on the genetic level,” said National Center for Genome Resources geneticist Stephen Kingsmore, co-author of the study published April 28 in Nature. The research cost $1.5 million, and the scientists took 18 months to sequence 2.8 billion DNA units in each twin, and determine whether they came from the mother or father. Most genomic comparisons look for differences in a just handful of suspect genes, and even whole-genome approaches don’t differentiate between parental contributions. The researchers also analyzed the twins’ CD4 cells, a type of white blood cell that plays a central role in the development of MS. In these cells, the researchers sequenced epigenomes — chemical instructions that turn genes on and off — and transcriptomes, or a chemical record of genes that are actively coding proteins. Wired.com © 2009 Condé Nast Digital.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 14023 - Posted: 06.24.2010

WASHINGTON - Under intense pressure from patients, some U.S. doctors are cautiously testing a provocative theory that abnormal blood drainage from the brain may play a role in multiple sclerosis — and that a surgical vein fix might help. If it pans out, the approach suggested by a researcher in Italy could mark a vast change for MS, a disabling neurological disease long blamed on an immune system gone awry. But many patients frustrated by today’s limited therapies say they don’t have time to await the carefully controlled studies needed to prove if it really works and are searching out vein-opening treatment now — undeterred by one report of a dangerous complication. “This made sense and I was hell-bent on doing it,” says Nicole Kane Gurland of Bethesda, Md., the first to receive the experimental treatment at Washington’s Georgetown University Hospital, which is set to closely track how a small number of patients fare before and after using a balloon to widen blocked veins. Story continues below ↓advertisement | your ad here In Buffalo, N.Y., more than 1,000 people applied for 30 slots in a soon-to-start study of that same angioplasty procedure. When the Buffalo General Hospital team started a larger study a few months ago just to compare if bad veins are more common in MS patients than in healthy people — not to treat them — more than 13,000 patients applied. The demand worries Georgetown neurologist Dr. Carlo Tornatore, who teamed with vascular surgeon Dr. Richard Neville in hopes of getting some evidence to guide his own patients’ care. © 2010 The Associated Press.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 13899 - Posted: 06.24.2010

CBC News It's long been thought that stress is harmful to your health, but a new study finds chronic stress may increase a person's risk of developing or accelerating a neurodegenerative disease like multiple sclerosis. Researchers have demonstrated for the first time that inflammation brought on by stress leads to the worsening of the mouse equivalent of MS. In studies, stressed mice produced a cytokine which is released during stress. That cytokine increased the severity of an MS-like illness in the mice. CBC The findings were presented Friday at the annual convention of the American Psychological Association. In the study, scientists simulated stressful situations on mice infected with Theiler's murine encephalomyelitis (TMEV), an acute infection of the central nervous system which is followed by a chronic autoimmune disease similar to that seen in humans with MS. Another group of mice was also infected but not exposed to stress. Researchers found that the stressed mice produced a cytokine — interleukin-6 (IL-6) — which is released during stress and regulates the part of the immune system that fights infection. IL-6 increases the severity of the MS-like illness. © CBC 2007

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 10622 - Posted: 06.24.2010

Heidi Ledford People with one of two common gene variants may be at increased risk of developing the autoimmune disorder multiple sclerosis (MS), researchers say. Both variants encode components of the immune system that are involved in preventing the body from attacking its own cells. Two papers1,2 published today in Nature Genetics independently pinpoint one of the variants, in the 'interleukin-7 receptor alpha chain' (IL7R) gene. A third research team scanned the full genome for variants associated with MS, and found both IL7R and another interleukin receptor gene — 'interleukin-2 receptor alpha' (IL2R) — among the top hits3. In MS the body's immune system attacks the insulating sheath that surrounds and protects neurons, leading loss of motor function and cognitive decline. Interleukin-2 and interleukin-7 are immune system proteins that play a role in the function of regulatory T-cells, which help suppress autoimmunity. The three research teams analyzed thousands of patients of European descent, and found that a single base pair difference in the IL7R gene increased the risk of having MS by about 20%. That risk is too low to make IL7R useful for a genetic test, cautions Margaret Pericak-Vance, a geneticist at the University of Miami in Florida, and an author on one of the studies. "A lot of people carry this particular variant, and they don't get multiple sclerosis," she says. Roughly 70% of the European population is likely to have the variant. ©2007 Nature Publishing Group

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 10544 - Posted: 06.24.2010

Researchers have found that patients with multiple sclerosis (MS) carry a population of immune cells that overreact to Epstein-Barr virus. The virus, which causes mononucleosis and may contribute to some cancers, has long been suspected to play a role in MS. However, the mechanism linking the virus to the disease was poorly understood. Scientists think that MS—which can cause vision problems, muscle weakness, and difficulty with coordination and balance—is a result of the immune system attacking the body's own nervous system. Not everyone who is infected with Epstein-Barr develops MS, but the results of the new study, published in the June 2006, issue of the journal Brain, suggest that some individuals' unusually strong reaction to the virus may trigger the disease. The findings could lead to new therapeutic strategies for better control of the damage caused in this autoimmune disorder. The culprit, the researchers say, may be a population of T cells that helps boost other components of the immune system in response to the virus. "What we discovered in the peripheral blood of the MS patients were T cells that appeared to be primed for action against EBV," said Nancy Edwards, an HHMI-NIH research scholar at the National Institutes of Health (NIH) and co-author of the paper, which was published in advance online. © 2006 Howard Hughes Medical Institute.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 8870 - Posted: 06.24.2010

When Ellen Bramble was 49 she stepped off a flight of stairs into thin air. She tumbled down, her laundry flying "every which way" and her limbs relaxed, as if she didn't even know she was falling. "I just kind of rolled and bounced on the concrete stairs…and I didn't get hurt, just a couple of bruises," says Bramble, a photographer from Portland, Oregon. This was the first of three falls that later led doctors to diagnose Bramble with multiple sclerosis (MS). MS is a disease in which the body's own white blood cells attack and erode the protective insulation around nerve fibers in the brain, spinal cord, and optical nerves, causing patients' bodies to go numb and lose track of what they're doing. As her disease progressed, Bramble, who is now 59, learned to deal with her physical limitations. But what's been most frustrating is that she's often felt lost in a "fog." Bramble has "cognitive dysfunction," a symptom shared by half of America's 400,000 multiple sclerosis patients, which makes it difficult for her to think clearly and to do simple things many people take for granted — remembering words, reading, keeping track of her daily chores, or even knowing where she's going when she pulls out of her driveway. (C) ScienCentral, 2000-2005.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 7430 - Posted: 06.24.2010

By Tia Ghose In people with autoimmune diseases like multiple sclerosis and asthma, infection-fighting cells go haywire and wage war against the body’s own tissue, causing inflammation. Existing treatments can prevent the immune system from getting out of control, but can also compromise a person’s ability to fight some infections. But a new study suggests that a specific receptor on immune cells holds promise as a target for treating such disorders, perhaps without affecting immunity. The receptor, called DR3, lies on the surface of T cells, which help the body combat infection. When a molecule called TL1A binds to the receptor, it spurs the T cells into action. But this same interaction can also lead the T cells to attack healthy tissue. Turning off the gene for this receptor seems to quell this inflammation in mice, researchers report online June 19 in the journal Immunity. It wasn’t far-fetched to think DR3 may play a role in autoimmune disease. DR3 is part of a family of TNF receptors, which are involved in activating immune cells and have been implicated in autoimmune disease, says Michael Croft, an immunologist at the La Jolla Institute for Allergy and Immunology in California, who was not involved in the study. What’s more, DR3 looks very similar to another receptor implicated in inflammation, says Richard Siegel of the National Institute of Arthritis and Musculoskeletal and Skin Diseases in Bethesda, Md, who was involved in the study. © Society for Science & the Public 2000 - 2008

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 11728 - Posted: 06.24.2010

By NICHOLAS WADE Medical researchers have made a significant advance in understanding multiple sclerosis, a common neurological disease that causes symptoms ranging from muscle weakness to paralysis. The disease is one in which the body’s immune system mistakenly attacks the electrical insulation of nerve fibers. The cause is part genetic and part environmental, but researchers trying to identify the relevant genes have endured repeated frustration. Their approach has been to guess what genes might be involved and see if patients have abnormal versions. This guesswork has produced more than 100 candidate genes in recent years, none of which could be confirmed except for long-known variants in the mechanism used by the immune system to recognize proteins that are foreign to the body. In three articles published online yesterday in The New England Journal of Medicine, three teams of researchers say they have identified, by separate routes, new genetic variants that contribute to the disease. One team used a new, advanced gene-hunting method called Whole Genome Association, which has racked up a string of successes with major diseases in the last few months. The other teams used the candidate gene approach, but because all three teams identified the same gene, the researchers say they are confident they have opened a new window into the cause and possible treatment of multiple sclerosis. Copyright 2007 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 10546 - Posted: 06.24.2010

Roxanne Khamsi A multiple sclerosis drug, voluntarily withdrawn from sale by its manufacturers following complications in patients, has shown substantial benefits in slowing the progression of the disease in a new study. Natalizumab (branded Tysabri), made by Biogen Idec and Elan Pharmaceuticals, reduced the risk of sustained progression of disability from MS by 42% in a study of about 1000 patients. Results from the two-year trial which began in 2001 and received supported by Biogen, were published in the New England Journal of Medicine on Wednesday. Natalizumab also decreased the frequency of clinical relapses, which could involve a dramatic reduction in sight or muscle function due to MS, by 68%. By comparison, current MS drugs on the market reduce these relapses by about one-third, comments Allan Ropper, at the Caritas-St. Elizabeth’s Medical Center in Boston, US, also an associate editor at NEJM. However, another study published alongside these results, following more than 3000 participants has estimated that patients treated with natalizumab have a one in 1000 chance of developing a potentially fatal disease of the central nervous system called progressive multifocal leukoencephalopathy (PML). PML, symptoms of which include mental deterioration and problems with speech, can be caused by a latent virus present in the kidneys of over 60% of people. The virus remains latent in healthy humans, but suppression of the immune system can allow it to become active and cause damage. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 8605 - Posted: 06.24.2010

A new pathway for treating multiple sclerosis may have been found, if “exciting” results in mice can be replicated in humans. MS is an incurable degenerative disease caused by the body’s immune system attacking the protective myelin sheath encasing the nerves that make up the central nervous system. The nerve fibres become increasingly damaged by scar tissue, known as sclerosis, which leads to paralysis and loss of speech and vision. But researchers trying a novel therapy on a mouse version of MS report that the mice showed “almost no inflammation of the myelin sheath and no nerve damage”. Furthermore, MS is characterised by periods of remission and relapse, but the mice recovered with fewer and far less severe relapses. The therapy targets immune system cells called T-cells. These malfunction in MS patients, producing inflammatory molecules that destroy the myelin sheath. The new treatment, which uses a class of molecules called kynurenines, works by inhibiting the T-cells’ production of inflammatory molecules and prompting them to produce agents that “mop up” the molecules. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 8107 - Posted: 06.24.2010

Possible insight to multiple sclerosis and other neurodegenerative diseases that destroy nerve cell 'insulation' In the May 3 issue of Science, scientists at Rockefeller University and New York University School of Medicine report that the nerve damage that leads to a loss of sensation and disability of people with leprosy occurs in the early stages of infection. The nerve damage, a hallmark of leprosy previously thought to be a byproduct of the immune system’s response to the leprosy bacteria, now seems to be a direct result of the leprosy bug attaching itself to specialized nerve cells called Schwann cells, the glial, or supporting, cells of the peripheral nervous system (PNS). The findings suggest that the body’s immune response does not play a significant role in the early stage of neurological injury.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 1998 - Posted: 06.24.2010

Lipitor ™ (atorvastatin), the most frequently used cholesterol lowering agent in the world, also has the ability to influence the immune system and proved effective in reversing paralysis in a mouse model of multiple sclerosis. Dr. Sawsan Youssef, a postdoctoral fellow in the laboratory of Dr. Lawrence Steinman, Stanford University, reported the study on April 23 at the Experimental Biology 2002 meeting in New Orleans. Multiple sclerosis is caused by the immune system attacking the body’s own central nervous system, breaking down the myelin that sheathes and protects CNS nerves, impairing the body’s ability to move normally, and eventually causing paralysis. The T lymphocytes of the mice with which the research team worked are sensitized to brain antigens so that they produce an over-abundance of cytokines, pro-inflammatory chemicals that inflame the CNS, causing demylination of nerve sheaths through the same mechanism and in the same manner as happens in human multiple sclerosis. As in humans with MS, this mouse condition (called experimental autoimmune encephalomyelitis or EAE) can occur in either an acute or relapsing form. The researchers found that oral treatment with lipitor could prevent both the acute and relapsing form of the multiple sclerosis-like disease in the mice, and could also reverse symptoms in mice with the ongoing chronic relapsing form of the disease.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 1929 - Posted: 06.24.2010