Hookworm trial offers new hope to MS patients

Parasitic worms could offer a new treatment hope for patients suffering from the autoimmune disease Multiple Sclerosis, according to experts from the University of Nottingham.

The findings of the research, published in the journal JAMA Neurology, show that infecting MS patients with a safe dose of the hookworm parasite Necator americanus induces immunoregulatory responses and boosts the number of cells which help keep the immune system under control.

The research was led by Cris Constantinescu, Professor of Neurology in the University's School of Clinical Sciences and a leading MS expert, and David Idris Pritchard, Professor of Parasite Immunology in the University's School of Pharmacy, who has spent decades studying the biology of the hookworm. The study was funded by the Multiple Sclerosis Society.

MS is a condition that can affect the brain and spinal cord, causing a wide range of potential symptoms, including problems with vision, arm or leg movement, sensation or balance. Whilst treatments are available, there is currently no cure.

The study aimed to show that the presence of hookworms in the body switches off the mechanism by which the body's immune system becomes overactive -- the main cause of MS -- reducing both the severity of symptoms and the number of relapses experienced by the patients.

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Scientists 're-train' immune system to prevent attack of healthy cells

The body's immune system can be re-wired to prevent it from recognising its own proteins which, when attacked by the body, can cause autoimmune diseases like Multiple Sclerosis, a significant new study by UK scientists has found.

Autoimmune diseases are caused when the immune system loses its normal focus on fighting infections or disease within and instead begins to attack otherwise healthy cells within the body. In the case of Multiple Sclerosis (MS), the body attacks proteins in myelin -- the fatty insulation-like tissue wrapped around nerves -- which causes the nerves to lose control over muscles.

Led by a multi-disciplinary team from the University of Birmingham, scientists examined the intricate mechanisms of the T-cells (or white blood cells) that control the body's immune system and found that the cells could be 're-trained' to stop them attacking the body's own cells. In the case of Multiple Sclerosis, this would prevent the body from attacking the Myelin Basic Protein (MBP) by reprogramming the immune system to recognise the protein as part of itself.

Supported by the Medical Research Council, the two-part study, published today in Cell Reports, was a collaboration between two research groups led by Professor David Wraith from the Institute of Immunology and Immunotherapy and Professor Peter Cockerill from the Institute of Cancer and Genomic Sciences.

The first stage, led by Professor Wraith showed that the immune system can be tricked into recognising MBP by presenting it with repeated doses of a highly soluble fragment of the protein that the white blood cells respond to. By repeatedly injecting the same fragment of MBP, the process whereby the immune system learns to distinguish between the body's own proteins and those that are foreign can be mimicked. The process, which is a similar type of immunotherapy to that previously used to desensitise people against allergies, showed that the white blood cells that recognise MBP switched from attacking the proteins to actually protecting the body.

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Mindfulness training shows promise for people with MS

New research suggests mindfulness training may help Multiple Sclerosis patients in two very different ways: regulating negative emotions and improving processing speed.

People with MS who underwent the four-week mindfulness training not only improved more compared to those who did nothing -- they also improved compared to those who tried another treatment, called adaptive cognitive training.

"This was a small pilot study, so we need to replicate the results, but these findings were very encouraging," said Ruchika Prakash, corresponding author of the research and associate professor of psychology at The Ohio State University.

"It is exciting to find a treatment that may be helpful in more than one way for people with Multiple Sclerosis."

The findings were published recently in two journal articles: primary results in Rehabilitation Psychology, and secondary analysis in Neuropsychology.

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Not all multiple sclerosis-like diseases are alike

An antibody appears to make a big difference between Multiple Sclerosis and other disorders affecting the protective myelin sheath around nerve fibres, report Tohoku University scientists and colleagues in the journal Brain. The finding suggests that some of these 'inflammatory demyelinating diseases' belong to a different category than Multiple Sclerosis, and should be treated according to their disease mechanism.

Multiple Sclerosis is a well-known demyelinating disease of the central nervous system, but is not the only one by far. In inflammatory demyelinating diseases,?targeted myelin sheaths -- the protective layers surrounding nerve fibres in the central nervous system -- becoming damaged, slowing or even stopping the transmission of nerve impulses. This leads to various neurological problems.

Scientists have found that some, but not all, patients with inflammatory demyelinating diseases have auto-immune antibodies against myelin oligodendrocyte glycoprotein (MOG), which is thought to be important in maintaining the myelin sheath's structural integrity. This antibody is rarely detected in patients with typical Multiple Sclerosis, but is found in patients diagnosed with optic neuritis, myelitis, and acute disseminated encephalomyelitis (ADEM), for example. Scientists had not yet been able to show that high levels of this antibody mean it is specifically targeting and damaging MOG.

Tohoku University neurologist Tatsuro Misu and colleagues in Japan analysed the brain lesions of inflammatory demyelinating disease patients with and without detectable MOG antibodies, and found the two groups were quite different.

Autopsies were taken from brain lesions of people diagnosed with Multiple Sclerosis and neuromyelitis optica spectrum disorder (NMOSD), which predominantly targets the optic nerve and spinal cord. These patients did not have detectable MOG antibodies. Typical Multiple Sclerosis lesions showed solitary, slowly expanding demyelination with a profound loss of myelin sheath proteins, and the presence of activated debris-clearing macrophages at their periphery. NMOSD lesions showed reductions in nerve cells called astrocytes and in myelin-producing cells called oligodendrocytes, and loss in the innermost layers of myelin sheath proteins.

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Living near major roads linked to risk of dementia, Parkinson's, Alzheimer's and MS

Living near major roads or highways is linked to higher incidence of dementia, Parkinson's disease, Alzheimer's disease and Multiple Sclerosis (MS), suggests new research published this week in the journal Environmental Health.

Researchers from the University of British Columbia analyzed data for 678,000 adults in Metro Vancouver. They found that living less than 50 metres from a major road or less than 150 metres from a highway is associated with a higher risk of developing dementia, Parkinson's, Alzheimer's and MS -- likely due to increased exposure to air pollution.

The researchers also found that living near green spaces, like parks, has protective effects against developing these neurological disorders.

"For the first time, we have confirmed a link between air pollution and traffic proximity with a higher risk of dementia, Parkinson's, Alzheimer's and MS at the population level," says Weiran Yuchi, the study's lead author and a PhD candidate in the UBC school of population and public health. "The good news is that green spaces appear to have some protective effects in reducing the risk of developing one or more of these disorders. More research is needed, but our findings do suggest that urban planning efforts to increase accessibility to green spaces and to reduce motor vehicle traffic would be beneficial for neurological health."

Neurological disorders -- a term that describes a range of disorders, including Alzheimer's disease and other dementias, Parkinson's disease, Multiple Sclerosis and motor neuron diseases -- are increasingly recognized as one of the leading causes of death and disability worldwide. Little is known about the risk factors associated with neurological disorders, the majority of which are incurable and typically worsen over time.

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Brain inflammation in veterans with Gulf War illness

In a new discovery, researchers at Massachusetts General Hospital (MGH) have detected widespread inflammation in the brains of veterans diagnosed with Gulf War Illness (GWI). These findings, published online in the journal Brain, Behavior, and Immunity on February 3, could serve as a guidepost for identifying and developing new therapies for people with GWI, as well as many other chronic conditions that have recently been linked to inflamed brain tissue, or neuroinflammation.

About 30 percent of soldiers who fought in the 1991 Gulf War suffer from GWI. Veterans with GWI display a range of symptoms, including fatigue, chronic pain and cognitive problems such as memory loss. The cause of GWI is unknown, but several potential culprits are suspected. They include exposure to nerve gas, as well as medicine given to protect against this neurotoxin; exposure to pesticides; and the stress of extreme temperature changes, sleep deprivation and physical exertion during deployment

Many of the symptoms of GWI overlap with those of another condition, fibromyalgia, notes the senior author of the study, Marco Loggia, PhD, whose laboratory at MGH's Athinoula A. Martinos Center for Biomedical Imaging focuses on understanding the brain mechanisms of pain and neuroinflammation in humans. Last year, Loggia and his colleagues showed in another study that fibromyalgia patients have extensive neuroinflammation. "So, we asked, Do veterans who have Gulf War Illness demonstrate evidence of neuroinflammation, too?"

To find out, Loggia and his team collaborated with the Gulf War Illness Consortium at Boston University, which helped them to recruit Gulf War veterans. The study included 23 veterans, of whom 15 had GWI, as well as 25 healthy civilian subjects. All study participants' brains were scanned using positron-emission tomography (PET) imaging, which measured levels of a molecule called translocator protein that rises in the presence of neuroinflammation. The scans detected little evidence of neuroinflammation in the healthy controls and veterans who were free of GWI. By contrast, the study found extensive inflammation in the brains of veterans with GWI, "particularly in the cortical regions, which are involved in 'higher-order' functions, such as memory, concentration and reasoning," says Zeynab Alshelh, PhD, one of two research fellows in Loggia's lab who co-led the study. "The neuroinflammation looked very similar to the widespread cortical inflammation we detected in fibromyalgia patients," says Alshelh.

What might cause neuroinflammation? The central nervous system has legions of immune cells that protect the brain by detecting bacteria, viruses, and other potentially harmful agents, then producing inflammatory molecules to destroy the invaders, explains Loggia. However, while this response can be beneficial in the short term, it may become exaggerated, says Loggia, "and when that happens, inflammation becomes pathological -- it becomes the problem."

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New injection technique may boost spinal cord injury repair efforts

Writing in the journal Stem Cells Translational Medicine, an international research team, led by physician-scientists at University of California San Diego School of Medicine, describe a new method for delivering neural precursor cells (NSCs) to spinal cord injuries in rats, reducing the risk of further injury and boosting the propagation of potentially reparative cells.

The findings are published in the Jan. 29, 2020 print issue.

NSCs hold great potential for treating a variety of neurodegenerative diseases and injuries to the spinal cord. The stem cells possess the ability to differentiate into multiple types of neural cell, depending upon their environment. As a result, there is great interest and much effort to use these cells to repair spinal cord injuries and effectively restore related functions.

But current spinal cell delivery techniques, said Martin Marsala, MD, professor in the Department of Anesthesiology at UC San Diego School of Medicine, involve direct needle injection into the spinal parenchyma -- the primary cord of nerve fibers running through the vertebral column. "As such, there is an inherent risk of (further) spinal tissue injury or intraparechymal bleeding," said Marsala.

The new technique is less invasive, depositing injected cells into the spinal subpial space -- a space between the pial membrane and the superficial layers of the spinal cord.

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The highways of our brain

Researchers from the Netherlands Institute for Neuroscience (NIN) used a new technique to show how electrical impulses are traveling with high speed in the brain. It appears that myelin, the sheath around neurons, creates a coaxial cable producing multiple waves of electrical potentials traveling in a more complicated manner than was envisioned earlier. These findings allow us to create better theories and tools to understand demyelinating diseases, including the most common neurological disorder, Multiple Sclerosis. The paper has been published in the scientific journal Cell.

The brain consists of around one hundred billion neurons. All these neurons have to communicate with each other. This happens by means of exchanging electrical impulses traveling at velocities of up to 360 km/h. "We know this requires the presence of myelin sheaths, consisting of multiple layers of fatty material wrapped around the nerve cell extensions. Myelin is often conceptualized as being an insulator that leads to the "jumping" of electrical potentials along the cables that we could see as the 'highways of our brain', but the mechanisms of jumping were not understood. However, this research opens new avenues to understand the hardware of the brain in terms of how they compute with rapid signal transfer," says professor Maarten Kole.

12 nanometers

Together with researchers of the Max-Planck Institute (MPI) of Experimental Medicine (Göttingen, Germany), the researchers used electron microscopy to measure the distance between the nerve cell membrane and the insulating sheath, which turned out to be 12 nanometers, approximately 10,000 times thinner than a hair. Furthermore, the scientists of the NIN used a new technique to make electricity visible and took advantage of a supercomputer to calculate the specific properties of myelin sheaths. "All the findings together showed that instead of being an insulating sheath, myelin creates an additional layer like coaxial cables producing multiple waves of electrical potentials travelling in a more complicated manner than was envisioned earlier," Kole explains. These findings open new avenues to understand the hardware of how brains are computing with rapid signal transfer.

Multiple Sclerosis

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Molecular switch for repairing central nervous system disorders

A molecular switch has the ability to turn on a substance in animals that repairs neurological damage in disorders such as Multiple Sclerosis (MS), Mayo Clinic researchers discovered. The early research in animal models could advance an already approved Food and Drug Administration therapy and also could lead to new strategies for treating diseases of the central nervous system.

Research by Isobel Scarisbrick, Ph.D., published in the Journal of Neuroscience finds that by genetically switching off a receptor activated by blood proteins, named Protease Activated Receptor 1 (PAR1), the body switches on regeneration of myelin, a fatty substance that coats and protects nerves.

"Myelin regeneration holds tremendous potential to improve function. We showed when we block the PAR1 receptor, neurological healing is much better and happens more quickly. In many cases, the nervous system does have a good capacity for innate repair," says Dr. Scarisbrick, principal investigator and senior author. "This sets the stage for development of new clinically relevant myelin regeneration strategies."

Myelin, Thrombin and the Nervous System

Myelin acts like a wire insulator that protects electrical signals sent through the nervous system. Demyelination, or injury to the myelin, slows electrical signals between brain cells, resulting in loss of sensory and motor function. Sometimes the damage is permanent. Demyelination is found in disorders such as MS, Alzheimer's disease, Huntington's disease, schizophrenia and spinal cord injury.

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Industry executives: Profits drive rising prices for MS drugs

U.S. Medicare patients with Multiple Sclerosis often pay, on average, nearly $7,000 out of pocket to treat their condition each year. And, even though drug companies have provided no new treatment breakthroughs, the price of these disease-modifying medications is rising by 10% to 15% each year for the past decade.

To find out why, a team of researchers at Oregon Health & Science University and the OHSU/Oregon State University College of Pharmacy recruited four pharmaceutical industry executives to speak confidentiality. In a study published today in the journal Neurology, the executives painted a frank picture of the rationale behind the price of medication available to people with MS.

"I would say the rationales for the price increases are purely what can maximize profit," one executive said. "There's no other rationale for it, because costs [of producing the drug] have not gone up by 10% or 15%; you know, the costs have probably gone down."

The executives acknowledged their companies' unique societal position in delivering medications to improve human health. However, each executive pointed out that their business model depends on generating a profitable return on investment to shareholders.

"The most surprising thing was how unsurprising it was," said lead author Daniel Hartung, Pharm.D., M.P.H., associate professor in the OHSU/OSU College of Pharmacy. "There was not this secret, complicated algorithm that these companies used to drive up prices."

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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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Novel PET imaging agent could help guide therapy for brain diseases

Date:Source:Society of Nuclear Medicine and Molecular ImagingSummary:Researchers have developed a new PET imaging agent that could help guide and assess treatments for people with various neurological diseases, including Alzheimer's, Parkinson's, and Multiple Sclerosis. The agent targets receptors in nerve cells in the brain that are involved in learning and memory.

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Researchers have developed a new imaging agent that could help guide and assess treatments for people with various neurological diseases, including Alzheimer's, Parkinson's, and Multiple Sclerosis. The agent, which is used in positron emission tomography (PET) scans, targets receptors in nerve cells in the brain that are involved in learning and memory. The study is featured in the April issue of The Journal of Nuclear Medicine.

Swiss and German scientists developed the new PET radioligand, 11C-Me-NB1, for imaging GluN1/GluN2B-containing N-methyl-D-aspartate (NMDA) receptors (a class of glutamate receptor) in nerve cells. When NMDA receptors are activated, there is an increase of calcium (Ca2+) in the cells, but Ca2+ levels that are too high can cause cell death. Medications that block NMDA receptors are therefore used for the treatment of a wide range of neurological conditions from depression, neuropathic pain and schizophrenia to ischemic stroke and diseases causing dementia.

"The significance of the work lies in the fact that we have for the first time developed a useful PET radioligand that can be applied to image the GluN2B receptor subunit of the NMDA receptor complex in humans," explains Simon M. Ametamey, PhD, of the Institute of Pharmaceutical Sciences, ETH Zurich, in Switzerland. "The availability of such a PET radioligand would not only help to better understand the role of NMDA receptors in the pathophysiology of the many brain diseases in which the NMDA receptor is implicated, but it would also help to select appropriate doses of clinically relevant GluN2B receptor candidate drugs. Administering the right dose of the drugs to patients will help minimize side-effects and lead to improvement in the efficacy of the drugs."

For the study, 11C-Me-NB1 was used in live rats to investigate the dose and effectiveness of eliprodil, a drug that blocks the NMDA GluN2B receptor. PET scans with the new radioligand successfully showed that the receptors are fully occupied at neuroprotective doses of eliprodil. The new radioligand also provided imaging of receptor crosstalk between Sigma-1 receptors, which modulate calcium signaling, and GluN2B-containing NMDA receptors.

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Our vulnerable nervous system: What affects its protective sheaths?

According to the Deutsche Multiple Sklerose Gesellschaft (German Multiple Sclerosis Society), around 200,000 people in Germany suffer from Multiple Sclerosis (MS) -- a serious neurological condition that has no known cure. Although the causes are far from being known, we do know that the the immune system erroneously attacks the protective sheaths around nerve fibres. In conjunction with researchers from Münster, Germany, a team of scientists at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) led by Prof. Dr. Michael Wegner have now discovered how the formation of myelin sheaths is regulated by protein molecules. This knowledge could be used to help MS patients by stimulating the formation of new myelin sheaths after a relapse.

The human brain is likened to a high-performance computer in which it's essential for the numerous individual processors to be connected to each other as efficiently as possible using high-speed cables. Each of the between 90 and 100 billion nerve cells represent the processors, and the nerve fibres or axons covered by myelin sheaths represent the fibre optic cables. The speed at which information is transmitted is highly dependent on the quality of the myelin sheaths, which are formed by special brain cells called oligodendrocytes. Damage to myelin sheaths or to the cells from which they are produced leads to serious disorders such as MS. Such disorders finally lead to the nerve cells being destroyed.

Complex mechanisms regulate myelin formation

The working group led by Prof. Dr. Michael Wegner, Chair of Biochemistry and Pathobiochemistry at FAU, is researching how oligodendrocytes regulate the formation of their myelin sheaths. Neurological disorders such as MS can only be understood with this knowledge. The working group has already identified protein molecules such as 'Sox10' that regulate the formation and preservation of myelin sheaths.

The aim of the new project was to understand how the identified proteins with the regulating function in the oligodendrocytes interact when myelin is formed. The researchers discovered that other molecules called Nfat proteins are required for this interaction between the known molecules to be successful. These are mainly known for their function in the immune system. The presence of Nfat proteins in the oligodendrocytes ensures that all other required protein molecules can exist together in these cells without displacing each other.

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First clues to the causes of multiple sclerosis

Multiple Sclerosis, which affects 1 in 1,000 people, is frequently characterised by relapses associated with variable functional impairments including among others vision problems, impairment of locomotor functions or difficulties with speech. There is still no cure for Multiple Sclerosis, with current treatments largely based on managing symptoms, especially accelerating recovery phases following a relapse and reducing the number and severity of relapses. Researchers at the University of Geneva (UNIGE), Switzerland, and Geneva University Hospitals (HUG) have identified a DNA-binding factor called TOX that might play a role in triggering Multiple Sclerosis. They found that TOX license immune cells to cause autoimmune tissue destruction in the brain. The results of the research, published in the journal Immunity, deliver important insights into our understanding and treatment of auto-immune diseases.

Multiple Sclerosis is as much of a mystery today as it has always been. We know that genetic risk factors but also environmental ones such as infection or even smoking are known to play a role in the development of the disease. However, it is still not known why it is triggered in some cases and not in others. "We decided to analyse the infectious factors by studying the auto-immune reactions provoked by different pathogens," explains Doron Merkler, Professor in the Pathology and Immunology Department in UNIGE's Faculty of Medicine and in the HUG Clinical Pathology Department. "This was to try to pinpoint an element that might influence the development of Multiple Sclerosis where there has been an infection."

Viral pathogen versus bacterial pathogen

The UNIGE researchers selected two distinct pathogens that elicit a response from the immune system -- one viral and one bacterial -- which were then injected into healthy mice. "We saw a quantitatively identical immune reaction from the lymphocytes called CD8+ T," says Nicolas Page, a researcher in UNIGE's Pathology and Immunology Department. "However, only the mouse infected with the viral pathogen developed an inflammatory brain disease reminiscent to Multiple Sclerosis."

Based on these outcomes, the scientists analysed how the expression of the genes in the CD8+ T cells varied according to the pathogen used to activate them. This helped them identify TOX, a DNA-binding factor expressed only in the cells activated by the viral pathogen. "We found that the inflammation environment influences the expression of TOX in T lymphocytes, and that it could play a role in triggering the illness," continues Page.

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How the gut influences neurologic disease

Researchers are identifying the key players involved in the gut-brain connection and their role in disease progression

Date:Source:Brigham and Women's HospitalSummary:A study sheds new light on the connection between the gut and the brain, untangling the complex interplay that allows the byproducts of microorganisms living in the gut to influence the progression of neurodegenerative diseases.

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A study published this week in Nature sheds new light on the connection between the gut and the brain, untangling the complex interplay that allows the byproducts of microorganisms living in the gut to influence the progression of neurodegenerative diseases. Investigators from Brigham and Women's Hospital (BWH) have been using both animal models and human cells from patients to tease out the key players involved in the gut-brain connection as well as in the crosstalk between immune cells and brain cells. Their new publication defines a pathway that may help guide therapies for Multiple Sclerosis and other neurologic diseases.

"These findings provide a clear understanding of how the gut impacts central nervous system resident cells in the brain," said corresponding author Francisco Quintana, PhD, of the Ann Romney Center for Neurologic diseases at BWH. "Now that we have an idea of the players involved, we can begin to go after them to develop new therapies."

The new research focuses on the influence of gut microbes on two types of cells that play a major role in the central nervous system: microglia and astrocytes. Microglia are an integral part of the body's immune system, responsible for scavenging the CNS and getting rid of plaques, damaged cells and other materials that need to be cleared. But microglia can also secrete compounds that induce neurotoxic properties on the star-shaped brain cells known as astrocytes. This damage is thought to contribute to many neurologic diseases, including Multiple Sclerosis.

Brigham researchers have previously explored the gut-brain connection to gain insights into Multiple Sclerosis. Although some studies have examined how byproducts from organisms living in the gut may promote inflammation in the brain, the current study is the first to report on how microbial products may act directly on microglia to prevent inflammation. The team reports that the byproducts that microbes produce when they break down dietary tryptophan -- an amino acid found in turkey and other foods -- may limit inflammation in the brain through their influence on microglia.

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Chemical compound produces beneficial inflammation, remyelination that could help treat multiple sclerosis

Chemical compound produces beneficial inflammation, remyelination that could help treat multiple sclerosis

Drugs available to treat Multiple Sclerosis, a leading cause of neurological disability affecting roughly 2.3 million people worldwide, alter the body's immune system to reduce disease symptoms and disability.

They do not induce, however, repair of damaged axons, the long threadlike parts of nerve cells that conduct impulses between cells or restore myelin, the protective sheath that surrounds the axons of neurons essential for the proper functioning of the brain and spinal cord.

Researchers at the University of California, Riverside, now report that indazole chloride, a synthetic compound that acts on one form of the body's estrogen receptors previously shown to reduce Multiple Sclerosis symptoms in mouse models, is able to do both: remyelinate (add new myelin to) damaged axons and alter the immune system.

"While additional translational studies are required, indazole chloride and similar drugs may represent a promising new avenue of treating the underlying loss of myelin in Multiple Sclerosis," said Seema Tiwari-Woodruff, an associate professor of biomedical sciences in the School of Medicine, who led the mouse study.

Multiple Sclerosis is triggered when the immune system attacks and damages the myelin sheath. As myelin is lost, nerve signals slow down or stop, affecting the patient's vision, movement, memory, and more. Oligodendrocytes are the mylenating cells of the central nervous system. Normally, oligodendrocyte precursor cells mature into myelin-producing oligodendrocytes when myelin is damaged.

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Mechanism controlling multiple sclerosis risk identified

While the DNA sequence remains the same throughout a person's life, the expression of the encoded genes may change with time and contribute to disease development in genetically predisposed individuals. Researchers at Karolinska Institutet in Sweden have now discovered a new mechanism of a major risk gene for Multiple Sclerosis (MS) that triggers disease through so-called epigenetic regulation. They also found a protective genetic variant that reduces the risk for MS through the same mechanism. The study is published in Nature Communications.

Multiple Sclerosis is a chronic inflammatory disease of the central nervous system, affecting people at a relatively young age. Most are between 20 and 40 years old when they get the first symptoms, in the form of, for example numbness in the arms and legs, visual impairment and dizziness, but also fatigue and depression. The symptoms are caused by an inflammation in the brain and the spinal cord that breaks down the myelin sheath protecting the nerves, thus damaging the axons. Currently there is no cure for MS, but the disease activity can often be halted through medication.

Already over 40 years ago it was discovered that genetic variation in the so-called HLA region is the strongest risk factor for developing disease. HLA encodes molecules that are involved in the immune system. However, the specific genes and molecular mechanisms behind the emergence of the disease are not fully established.

By using molecular analyses and combining several studies (so-called meta-analysis), including around 14,000 patients with MS and a control group of more than 170,000 healthy individuals, researchers at Karolinska Institutet found that people with the major risk variant HLA-DRB1*15:01 have an increased expression of the HLA-DRB1 gene, thus increasing the risk for the disease. The researchers further discovered a so-called epigenetic regulation of HLA expression as the mechanism mediating this effect.

"We show for the first time that epigenetic mechanisms can cause the disease. In addition, we can connect this mechanism to the genetic variant with the strongest risk for developing MS," says Maja Jagodic, researcher at the Department of Clinical Neuroscience at Karolinska Institutet and one of the authors of the article.

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Rethinking neurodegenerative disease treatment: Target multiple pathological proteins

Nearly all major neurodegenerative diseases -- from Alzheimer's to Parkinson's -- are defined and diagnosed by the presence of one of four proteins that have gone rogue: tau, amyloid-beta (Aβ), alpha-synuclein (α-syn), or TDP-43. As such, investigational drugs and studies aimed at preventing or slowing the disease often hone in on just one of these respective proteins. However, targeting multiple proteins -- known as "proteinopathies" -- at once may be the real key, according to a recent study published in Brain by Penn Medicine researchers.

These so-called "proteinopathies" -- misfolded proteins that accumulate and destroy neurons -- co-exist in varying degrees across all of the different neurodegenerative disorders and may instigate each other to drive disease severity in many aging patients. The prevalence of these co-pathologies suggests that each disease may ultimately require combination therapy targeting multiple disease proteins, and not just a single therapy, in patients with both early and later-stage disease.

"Historically, the focus of most clinical trials has been on targeting the primary pathological proteins of a given neurodegenerative disease such as deposits of tau and Aβ for Alzheimer's disease, but we see now that many of these disease-related aggregated proteins affect most older patients across a full spectrum of clinical and neuropathological presentations," said senior author John Q. Trojanowski, MD, PhD, a professor of Pathology and Laboratory Medicine and director of Penn's Institute on Aging. "This gives us additional leverage to find ways to detect patients' specific proteinopathies with increasingly sophisticated biomarker and imaging technologies. This will allow us, and other researchers, to better match participants with specific targeted therapies in clinical trials."

The study -- which analyzed 766 autopsied brains at Penn's Center for Neurodegenerative disease Research (CNDR) -- revealed that patients with more severe forms of their diseases had more co-pathologies. Researchers also found that increased age and the presence of the APOE ε4 allele -- a typical gene variant associated with an increased risk for late-onset Alzheimer's disease -- are risk factors for co-pathologies.

The researchers studied patients with the following diseases: Alzheimer's disease, Pick's disease, corticobasal degeneration (CBD), progressive supranuclear palsy, multiple system atrophy, Parkinson's disease with and without dementia, dementia with Lewy bodies, as well as frontotemporal lobar degeneration with TDP-43, amyotrophic lateral sclerosis, and primary age-related tauopathy (PART).

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Vitamin D no defense against dementia

New research from South Australian scientists has shown that vitamin D (also commonly known as the sunshine vitamin) is unlikely to protect individuals from Multiple Sclerosis, Parkinson's disease, Alzheimer's disease or other brain-related disorders.

The findings, released today in the science journal Nutritional Neuroscience reported that researchers had failed to find solid clinical evidence for vitamin D as a protective neurological agent.

"Our work counters an emerging belief held in some quarters suggesting that higher levels of vitamin D can impact positively on brain health," says lead author Krystal Iacopetta, PhD candidate at the University of Adelaide.

Based on a systematic review of over 70 pre-clinical and clinical studies, MS Iacopetta investigated the role of vitamin D across a wide range of neurodegenerative diseases.

"Past studies had found that patients with a neurodegenerative disease tended to have lower levels of vitamin D compared to healthy members of the population," she says.

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