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Tuesday, November 5, 2019

Potential genetic markers of multiple sclerosis severity

NEWS RELEASE 
In a bid to determine factors linked to the most debilitating forms of multiple sclerosis (MS), Johns Hopkins Medicine researchers say they have identified three so-called "complement system" genes that appear to play a role in MS-caused vision loss. The researchers were able to single out these genes -- known to be integral in the development of the brain and immune systems -- by using DNA from MS patients along with high-tech retinal scanning.
If further studies confirm the researcher's findings, reported in the September issue of Brain, the investigators say they could serve as markers for monitoring and predicting progression and severity of MS, an unpredictable disorder in which the immune system eats away at protective insulation around nerve cells. This approach, the researchers say, represents the beginning of precision medicine for MS and may ultimately allow designer therapies, as is being done for specific cancers.
In MS, nerve communication breaks down over time between the brain and the rest of the body, causing chronic and/or intermittent muscle spasms, tremors, imbalance, pain, numbness, depression, loss of bladder or bowel control and vision problems. MS is more common in women, and symptoms vary widely.
"Although we have treatments for the type of MS where symptoms come on in bursts -- called relapsing-remitting MS -- we don't have any way to stop the kind of MS in which the nerve cells start to die, known as progressive MS," says Peter Calabresi, M.D., professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and co-director of the Johns Hopkins Precision Medicine Center of Excellence for Multiple Sclerosis. "We believe that our study opens up a new line of investigation targeting complement genes as a potential way to treat disease progression and nerve cell death."
For their study, the researchers used optical coherence tomography -- an imaging technique that allowed the researchers to look at the back of each patient's eyes and assess damage to the nerve cells in the retina -- in 374 patients with all types of MS. The patients were an average of 43 years old and mostly women (78%).
The investigators recruited these patients and performed imaging every few years from 2010 to 2017, yielding an average of 4.6 scans per participant over the course of the study. The scans were used to measure thinning of the layer of the nerve cells -- known as ganglion cells -- in the retina over time. The average rate of deterioration was a loss of 0.32 micrometers of tissue per year in each patient.
Then, using blood samples from the patients to collect their DNA, the researchers hunted for genetic mutations in those people with the fastest deterioration rates and identified 23 such DNA variations that mapped to the complement gene C3.
Next, to search for genes further linked to vision loss, they performed an analysis of an existing clinical trial group of another 835 people with MS, of whom 74% were women, and whose average age was 40. Each participant underwent periodic vision testing about every year to distinguish their ability to detect contrast -- finer and finer shades that distinguish light versus dark. The test requires the person to read five letters in a row as with a typical vision chart test, as well as separate vison charts with faint (low contrast) letters that simulate vision in low light (dusk or dark). However, in this one each row down gets fainter and fainter rather than smaller and smaller.
Using DNA from the blood samples of these 835 participants, the researchers identified specific genetic changes in two complement genes, C1QA and CR1, linked to those people with the most rapidly declining ability to distinguish letters with less contrast. Patients with genetic changes in the C1QA gene were 71% more likely to develop difficulty detecting visual contrast, whereas those with genetic changes in the CR1 gene were at 40% increased risk for developing a reduced ability to detect contrast.
These complement genes found to be linked with severity of MS vision loss hold the genetic instructions for making complement proteins.
"Complement proteins have traditionally been thought of as part of the immune system, binding to antibodies and helping them kill infected cells in the body," says Calabresi. "A decade ago, however, other researchers discovered that complement proteins bind to the connections between neurons and helps them grow in specific directions. But, too much complement was found to causes damage to the nerve cells, eventually killing them. Our findings fit well into this system."
"Our next step will be to repeat these studies in larger populations," says Kathryn Fitzgerald, Sc.D., assistant professor of neurology at the Johns Hopkins University School of Medicine and first author of the published report. "Next, animal studies looking further into the function of complement proteins will also need to be performed so we can figure out the mechanism behind their role in killing nerve cells in people with MS. From there we can possibly think about how to design new therapies."

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Four (4) Remedies for MS fatigue and Cog Fog - video by Aaron Boster, MD

Got cog fog? MS fatigue? Well, stop these 4 things and improve your thinking, memory and energy levels! Learn to combat 2 of the most common Multiple Sclerosis symptoms!



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Aaron Boster, MD, Answering Viewers Questions: Fatigue & Depression in Multiple Sclerosis ·

Aaron Boster MD

In this video I answer viewers questions about two of the most common and difficult symptoms of Multiple Sclerosis, fatigue and depression. To learn more, start watching this vid right now!




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Monday, November 4, 2019

How new gene discoveries could guide precision medicine in multiple sclerosis

Eye
Variants in three "complement" genes are closely associated with vision loss in multiple sclerosis, Johns Hopkins Medicine researchers discovered. (Pixabay)
The most severe form of multiple sclerosis, called progressive MS, causes the death of nerve cells, which often leads to vision loss and other neurological problems. Now, scientists at Johns Hopkins Medicine say they’ve identified gene variants that play a role in MS-related vision loss—a discovery that could help guide precision medicine for treating the disease as well as the development of new therapies, they believe.

The Johns Hopkins team tied vision loss in MS to three “complement system” genes, which make proteins that are normally associated with immune function. Using gene testing, advanced imaging and vision tests on MS patients over seven years, the researchers discovered that variants in the genes, called C1, CR1 and C1QA, were closely associated with vision loss. They published the findings in the journal Brain.

“We believe that our study opens up a new line of investigation targeting complement genes as a potential way to treat disease progression and nerve cell death,” said Peter Calabresi, M.D., professor of neurology and neuroscience and co-director of the Johns Hopkins Precision Medicine Center of Excellence for Multiple Sclerosis, in a statement.

he team started by using optical coherence tomography to examine nerve cells in the retinas of 374 patients with MS. The scans allowed them to measure the thinning of the layer of those cells, which are known as ganglion cells, over time. Then they used blood samples from the patients to look for genetic mutations, pinpointing 23 variants in C3 in patients with the fastest rates of deterioration in ganglion cells.

A separate analysis of 835 patients who provided DNA samples and who underwent vision testing allowed the researchers to fine-tune their findings. They found that people with specific genetic variants in the complement gene C1QA were 71% more likely to lose their ability to detect visual contrasts over time, while those with changes in the CR1 gene faced a 40% risk of the same visual decline.

Several other research groups in MS are studying the role of genes and their variants in the progression and potential treatment of the disease. Early this year, a team at the University of Chicago found that a derivative of the hypertension drug Wytensin selectively inhibits a gene called PPP1R15A, which in turn seems to control inflammation in MS.

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