This Article is From Jun 16, 2009

Vitamin D gene may treat multiple sclerosis

Vitamin D gene may treat multiple sclerosis

AP image

Washington:

Scientists have discovered two new genes involved in multiple sclerosis, a breakthrough they claim could pave the way for treating the debilitating disease using Vitamin D.

An international team has pinpointed the two genetic variants which increase the risk of multiple sclerosis as well as reveal links to other autoimmune disease, the latest issue of the 'Nature Genetics' journal reported.

Lead scientist Professor Matthew Brown of the University of Queensland said: "One of the two genes is most likely a gene which controls metabolism of Vitamin D.

Previous research has already shown that levels of Vitamin D influence the risk of people contracting MS.

"For example, people have a higher risk the further they live from the Equator. This instantly suggests that a possible preventative treatment for MS is vitamin D. This may lead to new types of therapeutics down the track."

Their three-year study involved scanning the DNA of 1,618 people with MS and 3,413 people without MS.

The team looked at genetic landmarks in the genome called SNPs and then progressively narrowed down their search to individual genes.

After comparing over 300,000 SNPs, two genetic regions on chromosome 12 and 20 showed significant differences.

Changes in the region on chromosome 12 were discovered to coincide with an increased susceptibility to Type I diabetes and rheumatoid arthritis, whereas the region identified on chromosome 20 also coincided with susceptibility to rheumatoid arthritis and Graves' disease.

In addition, chromosome 12 encodes the enzyme that converts vitamin D, which one obtains mainly through sunlight, but also one's diet, into an active form that one's body can use, the study revealed.

"This advance in our understanding of genes involved in MS will eventually lead to more effective treatments. The next step in the research is to pinpoint the exact genetic mutations and the functional differences they are responsible for," said team member Simon Broadley of Griffith University.

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