MS linked to variant of common herpes virus

Researchers at Karolinska Institutet have developed a new method to separate between two different types of a common herpes virus (HHV-6) that has been linked to Multiple Sclerosis. By analyzing antibodies in the blood against the most divergent proteins of herpesvirus 6A and 6B, the researchers were able to show that MS-patients carry the herpesvirus 6A to a greater extent than healthy individuals. The findings, published in Frontiers in Immunology, point to a role for HHV-6A in the development of MS.

Multiple Sclerosis, MS, is an autoimmune disease that affects the central nervous system. The cause of the disease is unclear, but one plausible explanation is a virus tricks the immune system to attack the body's own tissue. Human Herpesvirus 6 (HHV-6) has previously been associated with MS, but in those studies it wasn't possible to distinguish between 6A and 6B. Through virus isolation from ill individuals, researchers have been able to show that HHV-6B can cause mild conditions such as roseola in children, but it has been unclear if HHV-6A is the cause of any disease.

According to estimates, as many as 80 percent of all children are infected with the HHV-6 virus before 2 years of age, and many also carry protection in the form of antibodies against this particular virus for the rest of their lives. But since it hasn't been possible to tell the two variants apart post-infection, it has been difficult to say whether HHV-6A or B is a risk factor for MS.

In this study, however, the researchers were able to distinguish between the A and B virus by analyzing antibodies in the blood against the proteins -- immediate early protein 1A and 1B (IE1A and IE1B) -- that diverge the most between the two viruses.

"This is a big breakthrough for both the MS and herpes virus research," says Anna Fogdell-Hahn, associate professor at the Department of Clinical Neuroscience at Karolinska Institutet and one of the study's senior authors. "For one, it supports the theory that HHV-6A could be a contributing factor to the development of MS. On top of that, we are now able, with this new method, to find out how common these two different types of HHV-6 are, something we haven't been able to do previously."

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Slowing the progression of multiple sclerosis

Date:Source:University of Montreal Hospital Research Centre (CRCHUM)Summary:Over 77,000 Canadians are living with Multiple Sclerosis, a disease whose causes still remain unknown. Presently, they have no hope for a cure. Researchers have now identified a molecule named ALCAM which, once blocked, delays the progression of the disease. Their results, obtained from in vitro human and in vivo mouse studies, could lead to the development of a new generation of therapies to treat this autoimmune disease.

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Over 77,000 Canadians are living with Multiple Sclerosis, a disease whose causes still remain unknown. Presently, they have no hope for a cure. In a study published in Science Translational Medicine, researchers at the University of Montreal Hospital Research Centre (CRCHUM) identify a molecule named ALCAM which, once blocked, delays the progression of the disease. Their results, obtained from in vitro human and in vivo mouse studies, could lead to the development of a new generation of therapies to treat this autoimmune disease.

Under normal conditions, the blood-brain barrier protects our brain from exposure to harmful elements. For example, it prevents cells of the immune system such as lymphocytes from invading our central nervous system. However, in people with Multiple Sclerosis, this barrier is permeable. A large number of lymphocytes manage to migrate into the brain and deteriorate its tissues (by destruction of the myelin sheath that protects the neurons and enables the transmission of nerve impulses).

"In our study, we show for the first time that a molecule called ALCAM (Activated Leukocyte Cell Adhesion Molecule), expressed by B cells, controls their entry into the brain via blood vessels. It allows them to migrate to the other side of the blood-brain barrier in mice and humans. By blocking this molecule in mice, we were able to reduce the flow of B cells into their brains and, as a result, slow the progression of the disease," said Dr. Alexandre Prat, a researcher at the CRCHUM, professor at the Université de Montréal and holder of the Canada Research Chair in Multiple Sclerosis.

B cells contribute to the progressive phase of Multiple Sclerosis. Certain medications, commonly known as anti-B-cell drugs, reduce its progression and the resulting disability.

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Surprise contributor to multiple sclerosis

Cells that scientists have largely ignored when studying Multiple Sclerosis are actually key contributors to MS development, new research from the University of Virginia School of Medicine shows. The discovery suggests new avenues for devising treatments and is a vital step toward finding a cure.

Understanding Multiple Sclerosis

Scientists had assumed that these cells, known as oligodendrocyte progenitor cells, could only serve a favorable role in MS. These glial cells make up about 5 percent of the brain and spinal cord, and they play an important and beneficial role by making cells that produce myelin -- insulation for nerve cells.

In MS, the body's immune system begins to attack the myelin, leading to a progressively disabling neurological condition that affects more than 2 million people worldwide. (MS is the most common neurological condition among the young, and is often diagnosed between ages 20 and 50.)

It has been thought that these progenitors do not efficiently give rise to myelin-producing cells in people with MS. Yet, UVA's Alban Gaultier, PhD, and his team made the surprising discovery that they are also actively participating in the immune system's harmful attacks on myelin.

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Genomic map implicates broad immune cell involvement in multiple sclerosis

The International Multiple Sclerosis Genetic Consortium (IMSGC) reports the results of its latest study, "Multiple Sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility," in the journal Science today: the highly productive collaborative group presents a new milestone in its efforts to understand the genetic basis of Multiple Sclerosis (MS). In a study of 115,803 individuals, the authors have identified 233 sites or loci in the human genome that contribute to the onset of MS. This is the largest study to date in MS and is based on the generous contribution of genetic material from 47,429 MS patients and 68,374 healthy individuals. The study's results confirm earlier results and offer a rich new perspective on the molecular events that lead some individuals to develop MS: it appears that dysfunction of many different immune cell types, both in the peripheral blood and the brain, contribute to triggering a cascade of events that ultimately leads to brain inflammation and neurodegeneration.

Dr. Philip De Jager, who directs the Multiple Sclerosis Center and the Center for Translational & Computational Neuroimmunology at Columbia University Irving Medical Center in New York City, and the principal investigator of the study says that "the study has created a detailed genetic map of MS, identifying over two hundred regions of the human genome that influence a large number of different immune cells, highlighting the fact that this disease is not caused by a single immune cell type but rather by a broad dysfunction of the immune system." MS has an initial inflammatory component and a secondary neurodegenerative component, so the investigative team looked closely at available data from human brain to assess whether changes in brain cells contribute to the onset of MS. Until now, it appeared that immune cells found in blood that come from the bone marrow played a critical role; the new study confirms this but also implicates microglia, the immune cells that live in the human brain. However, there is little evidence that other brain cells such as neurons that carry electrical signals in the brain are implicated in triggering MS.

Dr. Nikolaos Patsopoulos, Director of Systems Biology and Computational Science Program at the Ann Romney Center for Neurologic diseases of Brigham & Women's Hospital and Harvard Medical School in Boston, says that "our study explains approximately half of the heritability of MS, establishing MS as one of the well-characterized common diseases in terms of their genetic architecture." He adds that "this study highlights the complexity of the genetic contribution to MS susceptibility by identifying several regions of the genome with multiple genetic variants that play a small role. Further, we report the first ever association of genetic variant in chromosome X with MS, a disease that affects mainly young women. This study more than doubled our knowledge of MS genetics, however our findings suggest that there is more work to be done to fully understand how the human genome is involved in MS."

Dr. Tomas Olson, an author on the study from the Karolinska Institute in Stockholm, Sweden says that "this collaborative effort integrated multiple streams of North American and European funding to establish an important foundation for future projects that will uncover the sequence of events leading from health to MS. These genetic variants are not sufficient to cause MS; they interact with a host of environmental factors, making it more likely that a viral infection or other exposure triggers an autoimmune reaction against the brain and spinal cord."

Dr. Adrian Ivinson, Chief Operating Officer of the UK Dementia Research Institute who is also an author of this study adds that "this study reflects the combined, collaborative efforts of the international MS Genetics community to advance our understanding of MS disease mechanisms and the continuing support of the National MS Society in the completion of this project, the development of young investigators and support for basic research in MS. It is an excellent example for the success of collaborative team-oriented science in medicine."

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Researchers relate neuropsychological tests with real-life activity in multiple sclerosis

A recent review by Kessler Foundation researchers explored the relationship between neuropsychological assessment and predictability of performance of everyday life activities among people with Multiple Sclerosis (MS). The article, "Beyond cognitive dysfunction: Relevance of ecological validity of neuropsychological tests in Multiple Sclerosis," was epublished on August 30, 2019 by the Multiple Sclerosis Journal in a special issue on rehabilitation.

The authors are Erica Weber, PhD, and John DeLuca, PhD of Kessler Foundation, and Yael Goverover, PhD, of New York University, who is a visiting scientist at Kessler Foundation. Drs. Weber and Goverover are former Switzer fellows. The Switzer Fellowship is awarded by the National Institute on disability Independent Living and Rehabilitation Research to postdoctoral fellows with the potential to change the lives of people with disabilities though their research.

Individuals with neurological diseases such as MS often undergo neuropsychological testing to evaluate the influence of cognitive effects on their ability to perform everyday life activities. To be a useful tool for the clinicians who care for these individuals, it is important that their performance on neuropsychological testing parallels their function in everyday life. The Kessler team examined this issue, as well as the broader context for the question: "Are neuropsychological tests ecologically valid?"

The authors examined the literature on the relationships between cognitive and functional domains in the MS population. Cognitive functions included processing speed, executive function, visuospatial function, learning and memory, working memory, and verbal fluency. Functional domains included driving, employment, internet shopping and financial/medical decision-making.

They found that neuropsychological tests do have predictive value for individuals' behavior in these real life settings, according to Dr. Weber, research scientist in the Center for Traumatic Brain Injury Research. "While neuropsychological tests are ecologically valid in this population, other measures need to be considered in the clinical evaluation of individuals with MS, in order to understand the impact of the disease on everyday function," she explained. "Everyday life is complex, and there is no single measure for predicting the performance of complex daily activities. This is especially true for MS."

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AAN recommends people 65+ be screened yearly for memory problems

People with mild cognitive impairment have thinking and memory problems but usually do not know it because such problems are not severe enough to affect their daily activities. Yet mild cognitive impairment can be an early sign of Alzheimer's disease or other forms of dementia. It can also be a symptom of sleep problems, medical illness, depression, or a side effect of medications.

To help physicians provide the highest quality patient-centered neurologic care, the American Academy of Neurology (AAN) is recommending physicians measure how frequently they complete annual assessments of people age 65 and older for thinking and memory problems. This metric for yearly cognitive screening tests is part of an AAN quality measurement set published in the September 18, 2019, online issue of Neurology®, the medical journal of the American Academy of Neurology.

A quality measure is a mathematical tool to help physicians and practices understand how often health care services are consistent with current best practices and are based on existing AAN guideline recommendations. Quality measures are intended to drive quality improvement in practice. Physicians are encouraged to start small using one or two quality measures in practice that are meaningful for their patient population, and measure use is voluntary.

"Since thinking skills are the most sensitive indicator of brain function and they can be tested cost-effectively, this creates an enormous opportunity to improve neurologic care," said author Norman L. Foster, MD, of the University of Utah in Salt Lake City and a Fellow of the American Academy of Neurology. "The American Academy of Neurology is recommending the measurement of annual cognitive screenings for everyone age 65 and older because age itself is a significant risk factor for cognitive decline and mild cognitive impairment is increasingly prevalent with older age. The measure complements past American Academy of Neurology quality measures released for Parkinson's disease, Multiple Sclerosis and stroke, and allows for a doctor to meet the measure with a recommended periodic three-minute cognitive test."

According to the 2018 AAN guideline on mild cognitive impairment, nearly 7 percent of people in their early 60s worldwide have mild cognitive impairment, while 38 percent of people age 85 and older have it.

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New app offers faster and easier assessment for multiple sclerosis

Johns Hopkins Medicine researchers report they have developed and validated a tablet-based app that offers a faster, easier and more accurate way for health care providers who don't have specialized training to assess the cognitive function of people with Multiple Sclerosis (MS). Multiple Sclerosis is a chronic neurologic illness that affects the central nervous system, resulting in a variety of symptoms including motor issues, fatigue, visual disturbance, memory and concentration concerns, and mood changes.

MS is the most common form of disability in young adults other than traumatic injury. Diagnosis usually occurs between the ages of 20 and 50, and it is estimated that 1 million people in the United States are living with the disease. MS is most common among women -- three women are diagnosed for every one man.

In a study comparing the app, called iCAMS, to a standard, paper-based assessment tool, researchers say they found that the app produced highly accurate results while reducing test time from about 23 to 14 minutes. Study results are described in the July 2019 online issue of the International Journal of MS Care.

Meghan Beier, Ph.D., M.A., assistant professor of physical medicine and rehabilitation at the Johns Hopkins University School of Medicine and lead author of the study report, says that "results suggest that using the iCAMS app may make cognitive assessments of Multiple Sclerosis more convenient in a clinic setting, and therefore will be used more often to identify learning and memory problems."

According to Beier, up to 65% of people with MS experience cognitive problems. People with MS often require more time to perform mental tasks and face difficulty learning and retaining new information. Identifying cognitive issues earlier may help preserve and even improve function with targeted interventions such as cognitive rehabilitation, says Beier. Since cognitive decline can also be a result of aging, cardiovascular disease, depression and other conditions, specialized assessment tests have been developed to identify MS-related cognitive impairments. Certain exercises that improve learning ability, such as spaced learning and self-generated learning, may help MS-related cognitive difficulties. Therefore, it is important to identify these challenges.

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Social cognition, mood and fatigue in multiple sclerosis

A recent study by Kessler Foundation researchers linked the deficits in social cognition in Multiple Sclerosis with symptoms in other domains. The article, "Relationship between social cognition and fatigue, depressive symptoms, and anxiety in Multiple Sclerosis," was e-published on June 1, 2019 by the Journal of Neuropsychology.

The authors are Helen Genova, PhD, Katie Lancaster, PhD, Jean Lengenfelder, PhD, Christopher Bober, John DeLuca, PhD, and Nancy Chiaravalloti, PhD, of Kessler Foundation.

Researchers tested 28 individuals with Multiple Sclerosis for impairments of social cognition using tests of facial affect recognition and Theory of Mind, and looked for associations between deficits of social cognition with common conditions in this population by screening for fatigue, depression and anxiety. They also measured non-social cognitive ability, i.e., attention and processing speed, using the Symbol Digit Modality Test.

Preliminary findings showed consistent associations between poorer performance on measures of social cognition and increased symptoms of depression, anxiety, and fatigue, most notably psychosocial fatigue. Cognitive ability was not a factor in these associations.

The study raises issues of causality and reciprocal effects, according to Dr. Genova, the Foundation's assistant director of the Center for Neuropsychology and Neuroscience Research. "The nature of the relationships among these variables remains unclear," said Dr. Genova. "We cannot say whether deficits of social cognition worsen mood condition and fatigue, or vice versa," she explained. "The relationships may be reciprocal in nature," she observed. "Poor social cognition may worsen fatigue, depression and anxiety, leading to greater social isolation. That, in turn, may worsen social cognitive function."

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Medicare patients with multiple sclerosis bear the burden of rising drug prices

Over the course of a decade, out-of-pocket costs for Multiple Sclerosis drugs rose more than sevenfold for Medicare Part D beneficiaries, according to a JAMA Neurology study published today by researchers at the University of Pittsburgh.

Using Medicare claims data from 2006-2016, the researchers looked at trends in Multiple Sclerosis drug prices over time. Not only did they find steep increases in list prices -- the starting point before rebates, coupons or insurance kicks in -- but also in the ultimate costs to both Medicare and its recipients.

"We wanted to see how increases in list prices translated to increases in out-of-pocket spending, and we discovered that actual price increases do get passed down to patients, and that can negatively affect access," said study senior author Inmaculada Hernandez, Pharm.D., Ph.D., assistant professor of pharmacy at Pitt.

Several drugs on the market reduce the frequency and severity of Multiple Sclerosis flare-ups, which can involve a variety of disabling neurological symptoms, such as vision loss, pain, fatigue and muscle weakness.

From 2006-2016, the annual list prices of these drugs more than quadrupled, ballooning from about $18,000 to nearly $76,000 per patient per year.

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Vegetable-rich diet lowers fatigue in multiple sclerosis patients by raising good cholesterol

Higher levels of blood high-density lipoprotein (HDL) -- or good cholesterol -- may improve fatigue in Multiple Sclerosis patients, according to a new University at Buffalo-led study.

The pilot study, which investigated the effects of fat levels in blood on fatigue caused by Multiple Sclerosis, found that lowering total cholesterol also reduced exhaustion.

The results, published recently in PLOS ONE and led by Murali Ramanathan, PhD, professor in the UB School of Pharmacy and Pharmaceutical Sciences, highlight the impact that changes in diet could have on severe fatigue, which impacts the majority of those with Multiple Sclerosis.

Fatigue is a frequent and debilitating symptom for people with Multiple Sclerosis that affects quality of life and ability to work full time. Despite its prevalence and the severity of its impact, treatment options for fatigue are limited. The medications used to treat severe fatigue often come with unwanted side effects.

"Fatigue in people with Multiple Sclerosis has been viewed as a complex and difficult clinical problem with contributions from disability, depression and inflammation. Our study implicates lipids and fat metabolism in fatigue," said Ramanathan. "This is a novel finding that may open doors to new approaches for treating fatigue."

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Smoldering spots in the brain may signal severe MS

Aided by a high-powered brain scanner and a 3D printer, NIH researchers peered inside the brains of hundreds of Multiple Sclerosis patients and found that dark rimmed spots representing ongoing, "smoldering" inflammation, called chronic active lesions, may be a hallmark of more aggressive and disabling forms of the disease.

"We found that it is possible to use brain scans to detect which patients are highly susceptible to the more aggressive forms of Multiple Sclerosis. The more chronic active lesions a patient has the greater the chances they will experience this type of MS," said Daniel S. Reich, M.D., Ph.D., senior investigator at the NIH's National Institute of Neurological Disorders and Stroke and the senior author of the paper published in JAMA Neurology. "We hope these results will help test the effectiveness of new therapies for this form of MS and reduce the suffering patients experience."

Affecting more than 2 million people worldwide, Multiple Sclerosis is a disease for which there is no cure. The disease starts when the immune system attacks myelin, a protective coating that forms around nerve cells in a person's brain and spinal cord, to produce a variety of initial symptoms, including blurred or double vision, problems with muscle strength, balance and coordination, and abnormal sensations. Treatment with anti-inflammatory medications designed to quiet the immune system has helped some patients fully or partially recover. Nevertheless, a significant subset of patients will eventually suffer from a longer lasting, progressive form of the disease, which can cause further problems including paralysis, loss of bladder control and problems with attention, thinking, and memory.

Doctors often use magnetic resonance imaging (MRI) to diagnose patients as the immune system's attack produces lesions that appear as spots on scans of patients' brains. While some of the lesions heal, completely or partially, other lesions remain and rimmed ones appear to actively expand, or "smolder," for many years. Nevertheless, until recently, researchers did not fully understand the role chronic active lesions play in the disease, in part, because it was difficult to find the ones that remain chronically inflamed.

Starting in 2013, Dr. Reich's team showed that by using a high-powered, 7-tesla MRI scanner, they could accurately identify damaging, chronic active lesions by their darkened outer rims, in agreement with previous studies.

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Forgotten immune cells protective in mouse model of multiple sclerosis

A seldom-studied class of immune cells may reduce the friendly fire that drives autoimmune disease, according to a new study by researchers at the Stanford University School of Medicine. Stimulating these protective cells could lead to new therapies for diseases in which the immune system attacks the body's own tissues, such as Multiple Sclerosis and celiac disease.

In the study, to be published Aug. 7 in Nature, researchers tracked immune cells in the blood of mice with a disease akin to Multiple Sclerosis. They discovered a rise in CD8 T cells, typically known for killing infected or cancerous cells. To their surprise, injecting mice with peptides recognized by these CD8 T cells reduced disease severity and killed disease-causing immune cells.

While the bulk of the study was done in mice, the researchers also showed that one of their central findings -- an increase in CD8 T cells derived from single cells -- held true in cells from people with Multiple Sclerosis.

The findings suggest that inflammatory and suppressive immune cells balance each other like children on a seesaw. Selectively activating suppressive CD8 T cells during autoimmune disease may help restore that balance, said Mark Davis, PhD, professor of microbiology and immunology and the study's senior author.

"We absolutely think that something like this is happening in human autoimmune diseases. It represents a mechanism that nobody's really appreciated. There's this whole subset of CD8 T cells that has a suppressive function," said Davis, who holds the Burt and Marion Avery Family Professorship and is also a Howard Hughes Medical Institute investigator. "If we could mobilize those cells to function more effectively in patients with autoimmunity, then we'd have a novel treatment for diseases like Multiple Sclerosis."

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Cell types affected in brains of multiple sclerosis patients pinpointed

Scientists have discovered that a specific brain cell known as a 'projection neuron' has a central role to play in the brain changes seen in Multiple Sclerosis (MS). The research, published today in Nature, shows that projection neurons are damaged by the body's own immune cells, and that this damage could underpin the brain shrinkage and cognitive changes associated with MS. These new findings provide a platform for specific new MS therapies that target damaged brain cells to be developed.

Multiple Sclerosis is a disease of the brain and the spinal cord that affects over two million people worldwide. The potential symptoms of MS are wide ranging and can include problems with vision, movement and cognitive abilities. Previous research has shown that a brain region called the cortex shrinks over time in MS patients, known as cortical atrophy. The processes driving this cortical shrinkage have, until now, been unclear.

In a new international study from the University of Cambridge, University of Heidelberg and University of California, San Francisco, researchers used post-mortem human brain samples from MS patients to study a wide range of cell types implicated in the disease, and compared their findings to brain samples donated from people that did not have MS.

"Using a new technique called single nuclei RNA sequencing, we were able to study the genetic make-up of individual brain cells to understand why some cells might be more susceptible to damage in MS than others," said Dr Lucas Schirmer, lead scientist on the project from the University of Heidelberg.

"Our results showed that a particular type of nerve cell called "projection neurons" were particularly vulnerable to damage in the brains of MS patients."

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Gut microbes protect against neurologic damage from viral infections

Gut microbes produce compounds that prime immune cells to destroy harmful viruses in the brain and nervous system, according to a mouse study published today in eLife.

The findings suggest that having a healthy and diverse microbiota is essential for quickly clearing viruses in the nervous system to prevent paralysis and other risks associated with diseases such as Multiple Sclerosis.

A condition that causes progressive damage to nerve cells, Multiple Sclerosis has become more common over the past several decades. Viral infections in the brain or spinal cord are thought to trigger this disease. Some scientists believe that changes in the way we eat, increased sanitation or growing antibiotic use may be causing detrimental changes in the helpful bacteria that live within the human body, potentially increasing the risk of Multiple Sclerosis and other related diseases.

"We wanted to investigate whether gut microbes could alter the immune response to a virus in the central nervous system and whether this affects the amount of damage the virus causes," says one of the lead authors David Garrett Brown, a graduate research assistant in the Department of Pathology at University of Utah Health, Salt Lake City, US.

To do this, Garrett Brown and co-lead author Ray Soto looked at the effect of Mouse Hepatitis Virus, a virus that infects cells in the mouse nervous system and causes multiple-sclerosis type symptoms, on two groups of mice: some with normal gut microbes and some that were bacteria-free. They found that bacteria-free mice had a weak immune response, were unable to eliminate the virus and developed Worsening paralysis, while those with normal gut bacteria were better able to fight off the virus.

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Are the 'viral' agents of MS, ALS and schizophrenia buried in our genome?

What if the missing 'environmental' factor in some of our deadliest neurological diseases were really written in our genome?

Writing in Frontiers in Genetics, researchers from the University of Dusseldorf explain how viruses ended up in our DNA -- and what puts them in the frame in unsolved diseases like Multiple Sclerosis.

The enemy within

A whopping 8% of our DNA comes from viruses. Specifically, ones called retroviruses -- not because they're old, but because they reverse the normal process of reading DNA to write themselves into their host's genome.

Retroviruses are old though: they began merging with our earliest, primordial ancestors millions of years ago. Over the millennia, most of their remnants in our DNA -- known as human endogenous retroviruses or HERVs -- have been silenced by mutations. Others, which had evolved to fend off rival viruses, formed the prototypical immune system and to this day protect us from infection.

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Fooling nerve cells into acting normal

Fooling nerve cells into acting normal

Discovery could inform future studies related to spinal cord injuries, Multiple Sclerosis and epilepsy

Date:Source:University of Missouri-ColumbiaSummary:Scientists have discovered that a neuron's own electrical signal, or voltage, can indicate whether the neuron is functioning normally. If that voltage is absent, scientists say everything is 'out of whack.'

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Nerve cell illustration.

Credit: © peterschreiber.media / Adobe Stock

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Study shows promise in repairing damaged myelin

A scientific breakthrough provides new hope for millions of people living with Multiple Sclerosis. Researchers at Oregon Health & Science University have developed a compound that stimulates repair of the protective sheath that covers nerve cells in the brain and spinal cord.

The discovery, involving mice genetically engineered to mimic Multiple Sclerosis, published in the journal JCI Insight.

MS is a chronic condition that affects an estimated 2.3 million people worldwide. In MS, the sheath covering nerve fibers in the brain and spinal cord becomes damaged, slowing or blocking electrical signals from reaching the eyes, muscles and other parts of the body. This sheath is called myelin. Although myelin can regrow through exposure to thyroid hormones, researchers have not pursued thyroid hormone therapies due to unacceptable side effects.

Although several treatments and medications alleviate the symptoms of MS, there is no cure.

"There are no drugs available today that will re-myelinate the de-myelinated axons and nerve fibers, and ours does that," said senior author Tom Scanlan, Ph.D., professor of physiology and pharmacology in the OHSU School of Medicine.

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Do minerals play a role in development of multiple sclerosis?

Some studies have suggested that minerals such as zinc and iron may play a role in how Multiple Sclerosis (MS) progresses, once people have been diagnosed with it. But little was known about whether zinc, iron and other minerals play a role in the development of the disease. A new study shows no link between dietary intake of several minerals and whether people later develop MS.

The study is published in the April 3, 2019, online issue of Neurology®, the medical journal of the American Academy of Neurology. This article will also be published in the April 30 print issue of Neurology which is largely dedicated to null hypothesis studies with negative or inconclusive results. These results have the potential to inform future research efforts and to save study participants from avoidable risks.

"Higher intake of vitamin D has been associated with a lower risk of MS, but our findings show that intake of minerals is not an important determinant of MS risk," said study author Marianna Cortese, MD, PhD, of Harvard T.H. Chan School of Public Health in Boston.

The study involved 80,920 female nurses in the Nurses' Health Study and 94,511 in the Nurses' Health Study II. The women were asked via a questionnaire about diet and any supplement use every four years for up to 20 years of follow-up before some of the women developed MS.

The minerals studied were zinc, iron, potassium, magnesium, calcium, phosphorus, manganese and copper.

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Researchers optimize aptamer with enhanced myelin-binding properties for MS treatment

Date:Source:Mary Ann Liebert, Inc./Genetic Engineering NewsSummary:A new study has demonstrated the enhanced ability of an optimized 20-nucleotide derivative of a larger DNA aptamer to bind myelin in a mouse model of Multiple Sclerosis.

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-A new study has demonstrated the enhanced ability of an optimized 20-nucleotide derivative of a larger DNA aptamer to bind myelin in a mouse model of Multiple Sclerosis. The study, which also provides the first evidence of cross-reactivity of this myelin-binding aptamer with human brain cells, is published in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. Click here to read the full-text of this open access article on the Nucleic Acid Therapeutics website.

The laboratories of L. James Maher, III and Moses Rodriguez from Mayo Clinic College of Medicine and Science (Rochester, MN) coauthored the article entitled "Optimization of a 40-mer Antimyelin DNA Aptamer Identifies a 20-mer with Enhanced Properties for Potential Multiple Sclerosis Therapy." The researchers took a 20-nucleotide region of a parental 40-nucleotide myelin-binding DNA aptamer and used a rational, non-biased approach to molecular evolution to optimize the 20-nucleotide minimal sequence for improved myelin binding. They conclude that due to its cross-reactivity with human oligodendroglioma cells in vitro, it represents a promising lead molecule for further investigation.

"The authors highlight the value of aptamer refinement of a therapeutic for Multiple Sclerosis treatment and present a novel application for cell imaging," says Executive Editor Graham C. Parker, PhD, The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI.

Research reported in this publication was supported by the National Institutes of Health under Award Numbers T32GM065841 and F30CA220660. 

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Common treatment for multiple sclerosis may prolong life

Researchers from the University of British Columbia and Vancouver Coastal Health Research Institute have found that a widely prescribed drug for Multiple Sclerosis (MS) is associated with longer survival for patients.

The study, published today in the journal Brain, found that people with MS who took a beta interferon drug had a 32 per cent lower mortality risk than those that did not take the drug. This was particularly evident among MS patients who took beta interferon for more than three years.

The study, which followed nearly 6,000 people with MS in Canada and France over a period of more than two decades, is the first and largest of its kind to look at mortality associated with beta interferon for the treatment of MS.

"This is a significant study," said lead author Elaine Kingwell, a research associate and epidemiologist in the Djavad Mowafaghian Centre for Brain Health and the faculty of medicine at UBC, and Vancouver Coastal Health Research Institute. "Although these drugs have been prescribed since the mid-1990s, it takes time before scientists can look at the effect of these treatments on a long-term outcome like survival. We found that patients who were treated with these drugs during routine clinical practice survived longer overall than patients who had not taken beta interferon."

MS is a disease that affects the central nervous system, in which cells from the immune system attack and damage the nerve cells' protective sheath. The disease often results in disability and can have a significant impact on quality of life.

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