Researchers Discover New Gene Linked To Late-Onset Alzheimer's Disease
Alzheimer's disease not only affects the 5.8 million Americans diagnosed, but it also affects the friends and family members, who have to watch their loved one's health slowly decline. If you're related to the person suffering, an added fear of developing the disease yourself can lead to extra stress. This is because until now, scientists have had little understanding of how the disease is passed down genetically.
A study released in the Journal of Neuropathy & Experimental Neurology found a new gene, Mucin 6, that may contribute to late-onset Alzheimer's disease.
"Alzheimer's disease is a dreadful illness that mainly affects older persons, and there currently is no cure," Peter Nelson, M.D., Ph.D., and co-author of the study told mindbodygreen.
The high-heritability of the disease often goes ignored, according to Nelson, even though 60 to 80% of prior research proves that it can be genetic. The knowledge gap is known as "hidden heritability."
Until now, our technology hasn't been sophisticated enough to understand the complex human genome, but recent advances allowed Nelson and his team of scientists to conduct more precise studies on gene variation.
"There are regions of the human genome that have been effectively 'off-limits' to prior studies," Nelson said. "We looked into one of these regions and found a complicated gene change associated with Alzheimer's risk."
The study analyzed the data of 10,000 volunteers from the Alzheimer's Disease Sequencing Project to find out what genetic variations might be linked to late-onset Alzheimer's. That's how they found evidence of a link within a segment of the gene, Mucin 6.
If you're at risk for Alzheimer's disease, things like exercise, eating healthy, and reducing inflammation are a good idea to slow progression, but this new evidence led scientists one step closer to generating successful therapeutic strategies.
As for finding a cure? "That's where our future efforts will be aimed," Nelson told us.
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