Aging affects everyone, but some individuals experience it more rapidly than others. While some maintain their physical and mental capabilities into their 90s, others face health challenges like diabetes, Alzheimer's disease, or mobility issues at a younger age.
A recent study led by the University of Colorado Boulder, published in Nature Genetics, offers insights into why this happens. An international team of researchers identified over 400 genes associated with accelerated aging across seven different subtypes. These genes influence various aspects of aging, from cognitive decline to mobility issues and social isolation.
The study supports the "geroscience hypothesis," which suggests that addressing aging directly could help treat multiple chronic illnesses related to it.
"To develop treatments for accelerated biological aging, we must first understand its underlying biology," explained Isabelle Foote, the study's lead author and a postdoctoral researcher at CU Boulder. "This is the most extensive genetic study of frailty to date."
The research focused on "frailty," which describes multisystem physiological decline in older adults.
Over 40% of U.S. adults aged 65 and above are considered frail.
Doctors typically assess frailty using a score based on factors like walking speed, grip strength, health conditions, and social activity. However, two individuals with the same high score might have very different aging patterns—a cognitive decline in one could be matched by physical limitations in another.
"Frailty encompasses many aspects of aging," said Dr. Kenneth Rockwood, a leading expert on frailty based at Dalhousie University and co-author of the study. "The key question is: What genes are involved?"
To answer this, researchers conducted a genome-wide association study using DNA and health information from large datasets like the UK Biobank. They analyzed 30 different frailty symptoms, identifying 408 genes linked to accelerated aging.
Some genes were strongly linked to specific subtypes of unhealthy aging, such as SP1 for poor cognition or FTO for obesity-related issues.
"This study not only identifies types of unhealthy aging but also demonstrates the varied biology behind them," said senior author Andrew Grotzinger. "The next step is figuring out how to treat these underlying biological factors."
In practical terms, the authors suggest expanding frailty measurements in clinics to include six different subtypes.
This would allow for more personalized interventions—people with cognitive frailty could explore therapies to prevent dementia, while others with metabolic frailties might address risks of diabetes or heart disease.
Foote hopes for a future where individuals can receive "polygenic risk scores" that predict their likelihood of certain unhealthy aging patterns.
The ultimate goal is to identify and target the molecular pathways responsible for aging itself.
"A single anti-aging pill isn't on the horizon," Grotzinger comments, "but targeted treatments for specific age-related issues might be."