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Friday, February 5, 2016

Tiny but Dangerous: The Mosquitoes Spreading Zika

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Monday, February 1, 2016

MS Trigger Believed to Lie in Microglial Cells, Scientists Report

Researchers use gene analysis to identify specific cells as initiators of several brain disorders 


<span class="entry-title">MS Trigger Believed to Lie in Microglial Cells, Scientists Report</span><span class="entry-subtitle">Researchers use gene analysis to identify specific cells as initiators of several brain disorders</span>


Researchers have isolated the particular cell types likely to initiate common brain disorders and diseases, such as multiple sclerosis (MS) and Alzheimer’s disease, a finding that may point the way to new and targeted treatments.
The brain has a complex cellular architecture characterized by a diverse set of cell types that are highly interconnected. Identifying those involved with the pathogenesis of disease is particularly challenging in heterogeneous tissues where cell types are often poorly defined. In the majority of brain disorders, evidence exists for changes that affect multiple cell types.
In the study, titled “Identification of Vulnerable Cell Types in Major Brain Disorders Using Single Cell Transcriptomes and Expression Weighted Cell Type Enrichment” and recently published in the journal Frontiers in Neuroscience, scientists at the University of Edinburgh used an advanced gene analysis method, known as the Expression Weighted Cell-type Enrichment, to examine genes that switched on in certain types of brain cells. The information was then compared with genes known to be associated with conditions such as MS, Alzheimer’s, autism, schizophrenia and epilepsy, as well as anxiety disorders and intellectual disability.
Results showed that, for some of these diseases, support cells — rather than the neurons that transmit messages in the brain — are likely the first to be affected.


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Protein Seen to Impede Remyelination in Multiple Sclerosis Patients

Researchers from Karolinska Institute, Sweden, reported that the immune-associated protein lipocalin-2 (LCN2) is increased in multiple sclerosis, particularly in patients with progressive MS. The researchers, however, concluded that the factor cannot be used as a biomarker for the disease.
Initially identified as a peripheral immune factor, studies have recently suggested that LCN2 might play a role also in the central nervous system. Researchers believe it contributes to experimental autoimmune encephalitis, among other things, promoting demyelination. An earlier study also found increased levels of LCN2 in a small number of progressive MS patients, compared with patients with relapsing-remitting MS (RRMS)
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Nova radio announcer Katie Mattin opens up about her battle with MS

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Nova announcer Katie Mattin is living with MS. Picture: Jack Tran
KATIE Mattin knows what it’s like to need a positive role model.
That’s why the popular Nova 106.9 mornings announcer has decided to go public with her multiple sclerosis diagnosis for the first time since finding out seven years ago that she had the disease.
Mattin said she recently signed on as an ambassador for the MS Society of Queensland’s Brissie to the Bay bike ride in the hope of helping others who are living with MS to find their strength and courage.
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Can Cannabinoid Chewing Gum Treat Multiple Sclerosis Pain and Spasticity?


AXIM Biotech hoping for 2017 release of its pain-relief gum, MedChew Rx, moving into clinical testing
<span class="entry-title">Can Cannabinoid Chewing Gum Treat Multiple Sclerosis Pain and Spasticity?</span><span class="entry-subtitle">AXIM Biotech hoping for 2017 release of its pain-relief gum, MedChew Rx, moving into clinical testing</span>

MedChew Rx, by AXIM Biotechnology, Inc., the world’s first patented cannabinoid release chewing gum for pain and spasticity in multiple sclerosis (MS), is moving into clinical testing. If all goes well, the company plans for a global release date of 2017.
Medical cannabis is believed to have considerable promise as a therapy for difficult-to-treat pain associated with disorders like MS and other conditions that cause nerve pain. AXIM Biotech, based in New York and Ridderkerk, the Netherlands, says that if approved as expected by the FDA (U.S. Food and Drug Administration) and the EMA (European Medicines Agency), MedChew Rx — formulated with 5 mg of cannabidiol (CBD) and 5 mg of tetrahydrocannabinol (THC) — will be marketed as a pharmaceutical drug for treating MS.

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MS Cognitive Impairment Traced to Synapse Damage in Hippocampus




Researchers identified a new mechanism in the progression of multiple sclerosis (MS) that might explain the cognitive impairment and decline observed in these patients — a decline not directly associated with disease’s hallmarks of motor control loss, and one not currently addressed by the immunosuppressive drugs used to treat MS.
“For too long, MS has been characterized as a disease that impairs people’s mobility, speech, or vision,” Dr. Harris Gelbard, director of the Center for Neural Development and Disease at the University of Rochester Medical Center (URMC) and senior study author, said in a press release. “However, the aspect of the disease that many patients complain has the greatest impact on their quality of life is the loss of cognitive independence.”
In MS, cells of the immune system attack the central nervous system (CNS), namely myelin, the element that covers and protects nerve cells, and the nerve fibers themselves. CNS inflammation, demyelination, and axon loss are all hallmarks of the disease, which is mostly associated with motor and sensory symptoms. A large percentage of the MS patient population also experience some level of cognitive problems, such as memory loss and difficulty processing information. Because such cognitive impairment is not prevented through current therapies targeting immune system overactivation and myelin damage, the researchers theorized that additional damage was happening to CNS neurons located outside those brain areas known to be affected by myelin loss.


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Sunday, January 31, 2016

Study Shows That People with MS Taking Natalizumab Develop Antibodies to the JC Virus at Higher Than Normal Rates, Emphasizing Need for Regular Monitoring

January 27, 2016
  • A study by researchers in Germany and France observed changes in JC virus antibody status in two large groups of people with MS followed for 15 and 24 months. Having a positive antibody test to the virus means that a person has been exposed to the virus and has a higher risk of PML (a rare brain disease) than a person who has a negative antibody test, but a positive antibody test does not mean that a person has or will get PML.
  • The investigators found that a higher percentage of individuals’ blood tests changed from negative to positive in people treated with natalizumab than in people with MS who were not treated with natalizumab. They also found that levels (called the index) of antibodies in those who were already positive increased overall over time.
  • The results emphasize the need for vigilant monitoring of people with MS taking natalizumab, including regular antibody testing, MRI monitoring to improve detection of PML, and clinical monitoring for early signs suggesting the possibility of PML.
  • Decisions to initiate, continue or discontinue natalizumab need to include a conversation about the risk of PML, the risk of worsening MS and the potential adverse effects and the efficacy of alternative therapies.
  • The study, led by Heinz Wiendl, MD (University of Münster, Germany), was published January 27, 2016 in the online issue of Neurology Neuroimmunology and Neuroinflammation.
 
Background: Natalizumab (Tysabri,® Biogen) is given by infusion into the vein every four weeks. Although it can be very effective in reducing disease activity in people with relapsing MS, a small proportion of people taking Tysabri develop a rare brain disease called PML (progressive multifocal leukoencephalopathy). PML is caused by the activation of a virus called the JC (John Cunningham) virus. PML has also occurred in people taking other powerful immune-modifying therapies for MS, including fingolimod (Gilenya,® Novartis AG) and dimethyl fumarate (Tecfidera,® Biogen).
 
A blood test is available to test for the presence of antibodies (immune proteins), directed against the JC virus. Most people get this test before starting therapy with natalizumab, and every six months while they are taking it. Having a positive antibody test to the virus means that a person has been exposed to the virus and has a higher risk of developing PML than a person who has a negative antibody test. However, testing positive to JC antibodies does not mean a person has or will definitely get PML. Since the JC virus is common, generally about half of adults have antibodies to the JC virus. Research suggests that the expected rate of people in the general population changing (“seroconversion”) from antibody negative to antibody positive is about 1 percent per year.
 
Recent evidence also suggests that having higher  levels (called the index) of JC virus antibodies is an indicator of re-exposure to the virus or that the immune system is not fighting the virus adequately, which can further define risks of developing PML.
 
The Study:  This study observed changes in JC virus antibody status in two groups of people with MS: a group from Germany followed for about 15 months and a group from France followed for about 24 months. The investigators found that seroconversion rates in people treated with natalizumab were higher (from 8.5 to 10.3% per year) than those found in people with MS who were not treated with natalizumab. They also found that levels of antibodies in those who were already positive increased over time. This overall increase was largely the result of changes seen in  about 20 percent of the people observed; levels for the other 80% remained stable over the observation period.
 
The study, led by Heinz Wiendl, MD (University of Münster, Germany), was published January 27, 2016 in the online issue of Neurology Neuroimmunology and Neuroinflammation.
 
Comment: Although this study found seroconversion rates that were higher than expected among those taking natalizumab, and found an overall increase of antibody levels among those who were already antibody positive,
  • the majority who were negative at the start of the study were still negative after the observation period;
  • the majority of those who were JC virus antibody positive at the beginning of the study had stable levels of antibodies over the course of the study; and
  • the majority of individuals taking natalizumab who are JC virus antibody positive do not develop PML.
 
“This study emphasizes the need for vigilant monitoring of people with MS taking natalizumab, including regular antibody testing, MRI monitoring to improve detection of PML, and clinical monitoring for early signs suggesting the possibility of PML,” noted Bruce A. Cohen, MD, Professor, Davee Department of Neurology and Clinical Neurosciences at Northwestern University’s Feinberg School of Medicine, and Chair of the National MS Society’s National Medical Advisory Committee. “Natalizumab is a very effective disease-modifying therapy for relapsing MS, and any decision to discontinue this therapy in a person who is doing well on it needs to balance the risk of PML against their risk of worsening MS, and the potential adverse effects and efficacy of alternate therapies.”
 
Read the study and an editorial commenting on the study
Read prescribing information for natalizumab
 
NOTE: Prescribing information for natalizumab recommends that individuals taking this therapy call their healthcare provider right away if they experience any new or worsening medical problems that have lasted several days. These may be new or sudden and include problems with:  thinking; eyesight; strength; balance; weakness on one side of the body; using the arms and legs.
 
Gilenya is a registered trademark of Novartis AG.
Tysabri is a registered trademark of Biogen.
Tecfidera is a registered trademark of Biogen.
 


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Discover How Myelin-Making Cells Move Into Place – May Help Find Ways to Repair Myelin Damaged by MS

January 26, 2016
A team led by Dr. Stephen Fancy at the University of California, San Francisco, with collaborators at five other U.S. research institutions, conducted a series of studies to pinpoint how young cells with potential to make nerve-insulating myelin move into their proper places along blood supply routes in the developing brain. Since myelin is damaged during the course of multiple sclerosis, this basic discovery is likely to contribute to knowledge needed to find ways to repair myelin and restore function in people with MS.  Their discovery was published on January 22, 2016 in the journal Science.

Read more about this discovery
Read the abstract in the journal Science
Read more about research to repair the nervous system

complete article found here



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Potential Therapeutic Targets for Multiple Sclerosis Identified at MD Anderson


Jan 27, 2016  | Carolina Henriques


A study conducted by researchers at The University of Texas MD Anderson Cancer Center identified a protein regulator called Trabid as a key player on the complex chain of events that lead to autoimmune inflammation of the central nervous system (CNS) in patients with multiple sclerosis (MS). The study, “Epigenetic regulation of the expression of Il12 and […]








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