Latest Alzheimers News
TUESDAY, Dec. 5, 2017 (HealthDay News) -- Alzheimer's disease has long remained a deadly mystery.
But scientists say they've now pinpointed a rare piece of DNA that may shield against the illness -- even in people who are otherwise at high risk.
The discovery may explain why some people with known genetic risk factors don't develop Alzheimer's, the study authors said.
"There are currently no meaningful interventions for Alzheimer's disease -- no prevention, no modifying therapies, no cure," said study co-leader John Kauwe. He is a professor at Brigham Young University in Provo, Utah.
"The discoveries we're reporting in this manuscript provide a new target with a new mechanism that we believe has great potential to impact Alzheimer's disease in the future," Kauwe said in a university news release.
The finding came from analysis of the Utah Population Database, which included 20 million genealogical and historical medical records. The researchers identified families with a large number of people who had the main genetic risk factor for Alzheimer's -- E4 Allele -- but did not develop the disease.
The investigators then checked the individuals for DNA that they shared with each other but not with relatives who had developed Alzheimer's. The result was the discovery that the resilient people shared a variant in the RAB10 gene, while those who developed Alzheimer's did not have this gene variant.
The researchers then "over- and under-expressed" the gene variant in cells to assess its effect on Alzheimer's disease-related proteins.
Their conclusion: When this gene is reduced in the body, it appears to lower the risk for Alzheimer's.
According to study co-leader Perry Ridge, an assistant professor of biology at BYU, "Instead of identifying genetic variants that are causing disease, we wanted to identify genetic variants that are protecting people from developing disease. And we were able to identify a promising genetic variant."
The study was published online Nov. 29 in Genome Medicine.
-- Robert Preidt
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SOURCE: Brigham Young University, news release, Nov. 30, 2017
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