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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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