Identify genes associated with accelerated aging

Researchers have identified more than 400 genes associated with accelerated aging with the aim of developing therapies to slow it down, according to a study of the Colorado University Boulder.

Specifically, the study published in Nature Genetics It reveals that different genes of genes underlie different types of altered aging, also known as fragility, which cover from cognitive impairment to problems of mobility and social isolation.

“In order to identify treatments that stop or reverse accelerated biological aging, it is necessary Isabelle Fote. Thus, he adds that “this is the broader study to date that genetics uses to try to achieve it.”

The investigation focused on Identify what genes are involved in agingsomething complicated since it encompasses many conditions. Doctors often evaluate fragility through a 30 -point index that measures aspects such as walking speed, grip force, the number of diagnosed diseases and social activity. The problem, according to FOOTE, is that two people can obtain the same high fragility score even if one has cognitive acuity, but cannot walk, and another has good physical health but bad memory. “This lack of distinction has made it difficult for doctors to make recommendations and that scientists determine the underlying causes of unhealthy aging,” he says.

Therefore, to find out what genes are involved, the team conducted a “association study of the entire genome” Analyzing DNA and the health information of hundreds of thousands of participants in the BIOBANCO OF THE UNITED KINGDOM and other public data sets to see which genes were associated with 30 fragility symptoms. Thus, they identified 408 genes associated with accelerated/fragility aging, a significant increase with respect to the 37 genes previously identified.

With this, they discovered that some genes were strongly linked to certain subtypes of unhealthy aging, including: “disability”, “bad cognition”, “metabolic problems”, “multiple diseases”, “generally unhealthy lifestyle” and “limited social support”. For example, the SP1 gene, associated with the immune function and Alzheimer’s disease, was strongly associated with the broad subtype of “bad cognition”, while the FTO gene, a gene associated with obesity, seemed to be the basis of several different categories of unhealthy aging.

In this sense, in the short term, the authors suggest that clinical measurements of fragility (which often appears long before specific diseases) are extended to include six specific subtypes. In this way, someone diagnosed as cognitively fragile could be guided towards therapies to prevent dementia, while someone fragile in the metabolic domain could take measures to prevent diabetes or heart disease.

Thus, Foote imagines a day in which people could obtain a “polygenic risk score” that would offer a more detailed vision of what kind of unhealthy aging are prone.

The study concludes that “there will probably be not a single magical therapy to address all diseases that accompany aging, but perhaps it is no longer necessary to have hundreds of them.”