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Sunday, January 6, 2019

Can Biotin help treat MS?

Multiple sclerosis is an autoimmune disease in which the immune system attacks the central nervous system, including the brain and the spinal cord. Some studies suggest that a vital B-vitamin, biotin, might help reduce the impact of the disease.

By Danielle Dresden - December 2018
Reviewed by Zara Risoldi Cochrane, PharmD, MS, FASCP

Many people with multiple sclerosis (MS) use diet to help manage their symptoms. Many foods contain biotin, including brewer's yeast, nuts, egg yolks, Swiss chard, liver, and many others.

One important group of vitamins are the B-vitamins, which help the body turn food into energy, support the nervous system, and maintain the skin, hair, eyes, and liver. They are vital during pregnancy.

People sometimes refer to biotin as vitamin B-7 or vitamin H. It is one of the B-complex vitamins and is essential for human health.

The United States Food and Nutrition Board has not set a recommended daily allowance (RDA) for biotin, but the board has established an adequate intake (AI) level of 30 micrograms (mcg) per day for adults.

In this article, we look at the possible benefits of biotin in the treatment of MS.
Function


Amongst other foods, biotin can be found in nuts.

Biotin is thought to help manage presentations of progressive MS due to supporting nerve cell metabolism.

MS develops when the immune system targets and damages myelin, a substance that covers and protects the nerve cells. Biotin activates key enzymes, helping the body to produce more myelin.

Enzymes are proteins that carry out crucial functions in the body.

Healthy levels of myelin allow nerve cells to communicate with each other more efficiently. This communication between the nerve cells may reduce the level of disability in people with MS.

Producing more myelin may also slow the progression of the disease.

continue reading



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The role of friends and family when it comes to tracking MS symptoms

Tracking multiple sclerosis symptoms and progression can be very difficult. Sometimes a change in how you’re feeling is dramatic and impossible to miss. Unfortunately, I’ve found that many of my symptoms were much more subtle, and crept up slowly, so I wasn’t immediately aware of them. I unconsciously compensated for small changes I did not notice until things were more severe. That’s where others come in. 
My family and close friends all know I have MS, and my personal set of symptoms, and we occasionally talk about my condition. The subject isn’t taboo, but it doesn’t dominate the conversations either. It’s a fact of the life we live, but my life doesn’t revolve around MS.
When I was going through the Veterans Administration disability process, I was surprised to hear just how much weight a statement from one or more family members carried. When I asked about it, one of the VA representatives pointed out that someone can fake it all day at work, but the family sees the person when their guard is down and sees the impact. That has proven true for me.
My wife is my best observer and often notices the signs that I’m beginning to overheat or overexert myself before I recognize them. She was also the first to notice when I would repeat myself or pause to search for the right word. When she sees a behavioral change, she sometimes comments on it. The cause is often something other than MS, but I know she’s watching. Several years after I first showed symptoms, but before the diagnosis of MS, the “foot drop” in my right leg seemed to be shifting to my left leg as well. She also noticed that change before I did.
#msonetoone




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#BrainGames: Exercise your mind by playing these free puzzles and games


Training your brain with these games is a fun way to keep your mind active and focus on memory, concentration, and other brain skills.
Talk to your doctor if you experience any cognitive or other memory problems. He or she is always your best resource when finding ways to manage MS symptoms.
for:  Sudoko, Crossword and Flipout - click here


Mechanism of MS: A Complex Mosaic

https://www.msbrainpreservation.com/ms-pathogenesis/

A Closer Look at #MS Pathogenesis

The pathogenesis of multiple sclerosis (MS) involves a complex and dynamic interplay between the immune system and central nervous system (CNS) resident cells, including neurons and glial cells.1 These mechanisms contribute to the acute inflammation and diffuse neurodegeneration that characterize MS.1,2

The Role of Glial Cells

Neuroglia are a network of cells in the brain and spinal cord that support the CNS by maintaining homeostasis, producing myelin, and protecting neurons from outside attack.1,3,4
Glial cells include astrocytes, microglia, and oligodendrocytes.1
  • Astrocytes provide synaptic support, neuronal guidance, and maintain the blood-brain barrier3
  • Microglia have an important role in inflammatory and immune responses including clearing cellular debris and repairing tissues4
  • Oligodendrocytes create the myelin sheath that helps insulate axons and allows for efficient conduction of nerve impulses1

Glial Cell Activation

Glial cells are activated when immune cells, including T cells, cross the blood-brain barrier and set in motion a chain of cellular reactions.5-8
  • Cytokine Secretion: once inside the central nervous system, autoreactive T cells secrete proinflammatory cytokines1,8-10
  • Glial Activation: in response to these proinflammatory cytokines, resident glial cells such as microglia and astrocytes become activated3,8-10
  • Axonal Demyelination: activated microglia and astrocytes produce additional proinflammatory cytokines, such as TNF-α, NO, and IL-6, which play a key role in demyelination and axonal injury3,4,6,8,9
  • Oligodendrocyte Loss: inflammatory activity also results in the extensive loss and apoptosis of oligodendrocytes, which are no longer able to repair and replenish damaged myelin sheaths1,3,4

Glial Cell Activity in the Pathogenesis of MS1,3-10

Picture of Glial Cell Activity in the Pathogenesis of MS
Modified from Samuel S. Duffy, Justin G. Lees, and Gila Moalem-Taylor. The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis. Multiple Sclerosis International. Hindawi Publishing Corporation. © 2014. From an open access article distributed under the Creative Commons Attribution License, CC BY 4.0.

SOURCE



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The Art of Brain Preservation in Multiple Sclerosis

Adding Grey to the Palette Completes the Picture

What Is Brain Preservation?

Brain Preservation is a comprehensive look at neurological function that considers multiple factors contributing to central nervous system (CNS) damage in patients with multiple sclerosis (MS).
 

A Comprehensive Look at Multiple Sclerosis

Brain Preservation is a comprehensive look at neurological function that considers multiple factors contributing to central nervous system (CNS) damage in patients with multiple sclerosis (MS). It explores 4 areas related to brain and spinal cord damage, including
  1. White Matter pathology
  2. Grey Matter pathology
  3. Comorbidities/lifestyle
  4. Neurological Reserve

1. White Matter (WM): An important component of Brain Preservation in MS is preventing inflammatory lesions and volume loss (atrophy) in the WM of the brain.MS historically has been considered a disease of WM.1,2 Generally, there is a focus on preventing new inflammatory lesions, minimizing atrophy, and reducing the number of relapses experienced by MS patients. With every lesion prevented, there is a minimization of damage, beginning the process of Brain Preservation.3



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NEW RESEARCH might help to find an MS Cure: Gut Immune Cells Cut Inflammation in Multiple Sclerosis

Gut Immune Cells Cut Inflammation in Multiple Sclerosis

By Nicholas Weiler and Jim Oldfield on January 03, 2019


MRI scan of a person with MS.

Researchers at the University of Toronto and UC San Francisco have discovered that the intestine is the source of immune cells that reduce brain inflammation in people with multiple sclerosis (MS), and that increasing the number of these cells blocks inflammation entirely in a preclinical model of the disease.
The cells in question are plasma cells — white blood cells that originate as B cells in the bone marrow but change their behavior when triggered by microbes in the gut. Studying mice and samples from human MS patients, the researchers found that plasma cells that reside in the gut and produce Immunoglobulin A (IgA) antibodies appear to migrate to the central nervous system and produce an anti-inflammatory effect during MS flare-ups.
MS is an autoimmune disease, driven by other types of immune cells (including B and T cells) that attack myelin, the protective coating that surrounds nerve fibers. Recent clinical studies have shown drugs that target B cells mitigate MS, while those that target plasma cells make the disease worse. The current study offers an explanation for these divergent results.
“We already knew what was and was not working in the clinic,” said Jen Gommerman, PhD, a professor of immunology at the University of Toronto and the senior author on the study. “But here we’ve uncovered the molecular and cellular mechanism at play. It’s a kind of reverse translation approach, which highlights the importance of the gut-brain axis in MS and other autoimmune conditions.”
The results were published online January 3, 2019 in Cell.
Canada and the U.S. have among the highest rates of MS in the world, with around three in every thousand individuals affected. Symptoms can include fatigue, poor coordination, tingling, organ problems and cognitive impairment. There is no cure, although quicker diagnoses and better drugs have improved outcomes significantly in the last 15 years. 
“IgAs comprise 80 per cent of all antibodies in the body, yet their exact function is still not fully understood,” said Sergio Baranzini, PhD, a co-author on the paper who is a professor of neurology in the UCSF Weill Institute for Neurosciences. “Showing that IgA-producing B cells can travel from the gut to the brain opens a new page in the book of neuroinflammatory diseases and could be the first step towards producing novel treatments to modulate or stop MS and related neurological disorders.”
Sergio Baranzini smiling in his lab.
Sergio Baranzini, PhD, co-author of the study, UC San Francisco. Credit: Steve Babuljak.
Jen Gommerman and Olga Rojas side by side.
Study senior author Jen Gommerman, PhD, and co–lead author Olga Rojas, PhD, of the University of Toronto. Credit: Jim Oldfield / University of Toronto.
The lead authors on the work are postdoctoral fellows Olga Rojas, PhD, and Elisa Porfilio, PhD, from the Gommerman lab at the University of Toronto and Anne-Katrin Pröbstel, MD, from the Baranzini lab at UCSF. In a moment of scientific serendipity, they recently presented their research at the same conference and realized their results aligned. The researchers began to collaborate, and Pröbstel and colleagues in the Baranzini lab were able to show that the Gommerman lab’s findings in mice had parallels to human MS patients. 
Specifically, the UCSF team found evidence that IgA was decreased in fecal samples from patients with active MS neuroinflammation, suggesting that the inflammation-suppressing cells had been recruited to help fight the patients’ disease.
One promising aspect of the new research is that increasing the number of IgA plasma cells that migrate from the gut to the brain eradicated neuroinflammation in mice. A therapeutic approach might aim to expand the number of these cells in the gut, enabling a plentiful supply that could move to the brain and dampen inflammation. 
Anne-Katrin Pröbstel in the lab.
Anne-Katrin Pröbstel, MD, co-lead author of UC San Francisco. Credit: Sherman Jia.
“As a clinician-scientist, it is exciting that our experiments linking preclinical animal models to the biology we see in real MS patients may have uncovered a general mechanism for how the immune system counteracts inflammation,” said UCSF’s Pröbstel. “Until now, no one has really studied these IgA-producing plasma cells in the context of disease, but we are now examining them in detail in patients with MS to begin to understand how we might manipulate them to help treat neuroinflammatory disease.”
A key next step for the researchers is to figure out what microbes in the gut promote the generation of immunosuppressive IgA plasma cells. “If we can understand what these cells are reacting to, we can potentially treat MS by modulating our gut commensals,” said Gommerman, referring to the bacteria that live in the healthy gut. “That might be easier than getting drugs into the brain, which is a strategy that hasn’t always worked in MS.”


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Article Provided by Mitchell A. for #MSViewsandNews
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