Future therapies that could slow accelerated aging thanks to this discovery

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

Specifically, the study published in Nature Genetics reveals that different groups of genes underlie different types of altered aging , also known as frailty , ranging from cognitive decline to mobility problems and social isolation .

"In order to identify treatments that halt or reverse accelerated biological aging , we need to understand aging itself ," notes Isabelle Foote, the article's author and a postdoctoral researcher at the University of Colorado Boulder's Behavioral Genetics Institute. She adds, "This is the largest study to date that uses genetics to try to do this ."

The research focused on identifying which genes are involved in aging , a tricky process because it encompasses so many conditions. Doctors typically assess frailty using a 30-point index that measures things like walking speed, grip strength, number of diagnosed conditions, and social functioning. The problem, Foote says, is that two people can score equally high on frailty, even if one is cognitively sharp but unable to walk, and another is physically healthy but has a poor memory. "This lack of distinction has made it difficult for doctors to make recommendations and for scientists to determine the underlying causes of unhealthy aging," she notes.

So, to find out which genes are involved, the team conducted a " genome-wide association study, " analyzing the DNA and health information of hundreds of thousands of participants in the UK Biobank and other public datasets to see which genes were associated with 30 symptoms of frailty. They identified 408 genes associated with accelerated aging /frailty, a significant increase from the 37 genes previously identified.

In doing so, they found that some genes were strongly linked to certain subtypes of unhealthy aging, including: "disability," " poor cognition ," "metabolic problems," "multiple diseases," "generally unhealthy lifestyle," and "limited social support." For example, the gene SP1, associated with immune function and Alzheimer's disease , was strongly associated with the broad subtype of "poor cognition," while the gene FTO , a gene associated with obesity , appeared to underlie several different categories of unhealthy aging.

In this regard, in the short term, the authors suggest that clinical measurements of frailty (which often appears long before specific diseases) be expanded to include six specific subtypes. That way, someone diagnosed as cognitively frail could be guided toward therapies to prevent dementia, while someone who is metabolically frail could take steps to prevent diabetes or heart disease.

So Foote envisions a day when people could get a " polygenic risk score " that would offer a more detailed view of what kind of unhealthy aging they are prone to.

The study concludes that "there probably won't be a single magic bullet to address all the diseases that accompany aging, but hundreds of them may no longer be necessary."