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Archive for the tag ““MS Focus”

28 Jul 2016

Study suggests antibody may have therapeutic effect on MS

Researchers have developed an antibody with potential therapeutic effects against multiple sclerosis. The discovery opens up a new strategy for controlling the disease.

For the cells of the immune system circulating in the bloodstream to reach the central nervous system, they must penetrate the blood-brain barrier and blood-spinal cord barrier. During previous work, the authors studied a factor involved in opening the blood-brain barrier, the NMDA receptor. They found that blocking the interaction of this receptor with tPA has beneficial effects linked with maintaining the integrity of the barrier.

Scientists at the Institut National de la Santé et de la Recherche Médicale, in France, developed a monoclonal antibody (Glunomab) directed against the specific site on the NMDA receptor to which tPA binds. In cellular models of the human blood-brain and blood-spinal cord barriers, the use of this antibody prevented opening of the barrier under inflammatory conditions, limiting the entry of lymphocytes. The team then tested the therapeutic effects of the antibody in an experimental mouse model of MS. After intravenous injection of Glunomab, the progression of partial or total paralysis of the limbs – as assessed by a clinical score – was blocked. In these treated mice, this effect was linked with reduced infiltration of lymphocytes into the nervous tissue, and reduced demyelination.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the authors argue that by preventing myelin destruction by the cells of the immune system, this strategy might represent a promising therapy for the control of MS.

The study was published in the journal Brain.

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10 Apr 2016

Study finds greater role for environment in MS

Environmental factors may be playing a much greater role in the onset of multiple sclerosis than previously realized, according to early research led by Queen Mary University of London and Barts Health NHS Trust. The theory is based on new findings showing that Black people and South Asians in east London have a higher prevalence of MS compared to those groups in their ancestral countries, indicating a strong environmental influence on the disease that could be driving higher MS rates in London.

The researchers, led by Dr. Klaus Schmierer, used electronic records from general practices in four east London boroughs (Tower Hamlets, Newham, Hackney and City of London) which were reviewed for the number of MS-diagnosed patients, grouped by ethnicity. What they found was that MS appeared to be several times more prevalent among African people and South Asians living in London compared to those groups living in their ancestral territory. While prevalence differences could be explained by fewer MS diagnoses occurring in less resourced countries, the authors said it is unlikely to explain the gulf in prevalence between these territories. They said that an alternative, or additional, explanation would be increased exposure in the UK to environmental agents or behaviors that facilitate the development of MS.

Lead author Schmierer said, “MS is a disease where genetic ancestry and environmental factors play a role, however to what degree these two aspects are driving the risk of developing MS remains unknown. We found that people of Asian and African extraction in London are far more likely to have MS than people of the same ethnicity living in their ancestral countries. Our early results suggest that environmental factors play a pivotal role in the risk of developing MS, while the individual genetic backdrop may be of lesser importance.”

The study was published in Multiple Sclerosis Journal.

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17 Nov 2015

Researchers seek volunteers for self-compassion survey

Oregon State University researchers are seeking participants for an online survey to investigate the relationship of self-compassion on resilience, physical activity, and quality of life for individuals with MS.
Subjects between the ages of 18 and 65 who can communicate in English and have a medical diagnosis of MS are eligible to participate in this study. The survey takes 20 to 30 minutes to complete. Participation in the survey is voluntary. Personal identification information will be removed from the survey data.
Survey answers will help improve understanding of the process of self-compassion and physical activity on improving health-related quality of life for individuals with MS. Results from this study will also help researchers develop effective health interventions to improve wellness and quality of life for people with MS.
To complete the survey, visit http://oregonstate.qualtrics.com/SE/?SID=SV_8ktgzQ9Jki71UEt
If you are interested or have any questions, contact the research team at nerym@onid.oregonstate.edu.

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08 May 2015

Researchers implicate chemical in MS

A new study confirms that the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF) likely plays an important role in multiple sclerosis. Researchers also offer a new explanation for why the MS treatment interferon-Beta (INF-β) is often effective at reducing attacks.

Researchers, led by Abdolmohamad Rostami, M.D., Ph.D., Chair of the Department of Neurology at Thomas Jefferson University and director of its neuroimmunology laboratory, tested blood samples of patients with MS who had not yet received therapy, and those currently being treated with INF-β, a commonly used therapy. On average, untreated patients had two to three times as many immune cells producing GM-CSF as did patients being treated with INF-β, or normal subjects. Researchers looked at brain samples of deceased patients with MS and found increased numbers of GM-CSF-producing cells in comparison to normal brain samples.

“Abundant GM-CSF production at the sites of CNS inflammation suggests that GM-CSF contributes to MS pathogenesis. Our findings also reveal a potential mechanism of IFN-β therapy, namely suppression of GM-CSF production,” the authors said.

The findings were published online in the Journal of Immunology.

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28 Mar 2015

New molecule may lead to inflammation inhibitor

Scientists have developed a new drug-like molecule that can inhibit inflammation. The find has shown promise in preventing the progression of multiple sclerosis.
Walter and Eliza Hall Institute scientists have developed a small drug-like molecule called WEHI-345 that binds to and inhibits a key immune signaling protein called RIPK2. This prevents the release of inflammatory cytokines. Examining WEHI-345’s potential to treat immune diseases in experimental models of MS, it was found that WEHI-345 prevented further progression of the disease in 50 percent of cases after symptoms of MS first appeared.
Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. Calling the results extremely important, researchers said WEHI-345 had potential as an anti-inflammatory agent.
The study’s lead author, Dr Ueli Nachbur, said institute scientists would use WEHI-345 to further investigate the signaling pathway that produced inflammatory cytokines and to develop a better, stronger inhibitor of RIPK2 for treating inflammatory disease. “This signaling pathway must be finely balanced, because WEHI-345 only delayed signaling rather than blocked it. Nevertheless, this delay is enough to completely shut off cytokine production,” he said.
The research was published in the journal Nature Communications.

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08 Mar 2015

Study: Genetic variant may be MS risk factor

In a new study, researchers testing DNA in siblings with MS discovered a genetic variant in women that may increase risk of developing multiple sclerosis. According to study authors, the variant may be the one of the strongest genetic risk factors for MS discovered to date.

Researchers at the University of Illinois at Chicago were able to test three sisters among a group of five siblings between the ages of 23 and 26, all diagnosed with MS. What they found was a genetic change known as a single nucleotide polymorphism, or SNP – a change in a single base-pair of the DNA – in a gene called STK11, which plays a role in tumor suppression and is believed to have several roles in brain function. They found the variant in all three they tested.

To determine if the SNP could be a contributing factor to the siblings’ multiple sclerosis, the researchers screened DNA samples from 1,400 people – 750 with MS and 650 without – provided by Jorge Oksenberg at the University of California, San Francisco, who is a leading expert on the genetics of MS. They found that the SNP was 1.7 times as prevalent in women with MS as in women without the disease, making it one of the highest known genetic risk factors for MS.

Based on their analysis, the researchers estimate that the STK11 SNP is present in about 7 percent of the general population. But because far fewer people develop MS, other genetic or nongenetic factors must play a role in the development of the disease, said senior author Doug Feinstein, professor of anesthesiology at UIC and research biologist at the Jesse Brown VA Medical Center.

The variant occurs almost twice as often among women with MS as in women without the disease, making it “one of the strongest genetic risk factors for MS discovered to date,” said Feinstein.

The findings were published in the journal ASN Neuro.

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25 Jun 2012
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Study Identifies Gene Linked to Vitamin D Deficiency

A recent study at Oxford University in England and published in Annals of Neurology, has identified a gene that causes vitamin D deficiency, a condition suspected of having a role in the development of MS.

The study examined the DNA of a group of people with MS who also have a large number of family members with the disease. All the DNA samples showed a distortion of the CYP27B1 gene which controls vitamin D levels in the body. And in a few rare cases where the DNA showed two copies of the distorted gene, the person was found to have a genetic form of rickets caused by vitamin D deficiency as well as MS.

The cause of myelin damage related to MS is still hotly debated: some believe it to be an autoimmune disease while others cite viruses or the environment as the culprit. There is growing evidence however of a correlation between MS and vitamin D deficiency. Epidemiological studies also show that populations closer to the equator and the sun, have far fewer case of MS than populations closer to the north or south poles. Researchers at Oxford University have now taken this premise a step further by showing that vitamin D deficiency and therefore possibly MS could have a genetic cause.

Despite this pivotal link, not all people with vitamin D deficiency develop MS. More research is needed to fully understand why. However, a distortion of the CYP27B1 gene is increasingly apparent in MS cases and it’s possible that the gene generates other, yet undetected, complications that lead to the disease—such as genetically caused rickets.

“Although vitamin D deficiency doesn’t always cause MS, it unveiled a critical genetic source that could be causing other problems that lead to MS,” says Jeffrey Epstein, whose foundation partially supported the study. “Even if we don’t understand all of the implications of that gene’s distortion, research can focus on gene therapy, and that will accelerate a cure.”

The study was partly funded by the National Multiple Sclerosis Society, The Wellcome Trust and the support of science investor, Jeffrey Epstein and The Jeffrey Epstein VI Foundation.

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