We’ve all seen it: Some people reach their 90s with their memory sharp and their bodies strong, while others face diabetes, Alzheimer’s disease, or mobility problems decades earlier.
Why do some people age so much faster than others? New research led by the University of Colorado Boulder offers some important answers.
The study, published in Nature Genetics, involved an international team of scientists who analyzed DNA and health information from hundreds of thousands of people.
They discovered more than 400 genes linked to accelerated aging—ten times more than were previously known.
The findings suggest that different groups of genes drive different kinds of unhealthy aging, ranging from memory loss to poor physical health to social isolation.
The results support the “geroscience hypothesis,” which argues that to fight the chronic illnesses of old age, we need to treat aging itself.
“To stop or slow down accelerated biological aging, you first need to understand the biology behind it,” said Isabelle Foote, lead author and postdoctoral researcher at CU Boulder’s Institute for Behavioral Genetics.
The study focused on the concept of “frailty,” a broad term used to describe the physical and mental decline that comes with age.
More than 40% of Americans over 65 are considered frail, but frailty can mean very different things. Doctors often measure it with a checklist of about 30 indicators, including walking speed, grip strength, number of illnesses, and levels of social activity.
The problem is that two people can receive the same frailty score for very different reasons—one may be physically weak but mentally sharp, while another may be physically fit but experiencing memory problems.
To dig deeper, the team used a “genome-wide association study” to scan DNA for patterns linked to these traits.
They found 408 genes tied to different forms of accelerated aging. Some genes were connected with specific problems: for example, the SP1 gene, linked to immune function and Alzheimer’s disease, was strongly associated with cognitive decline, while the FTO gene, often tied to obesity, was linked to several types of unhealthy aging.
“This paper shows that there are many ways to be frail, and very different biology underlies each one,” explained senior author Andrew Grotzinger, assistant professor of psychology and neuroscience at CU Boulder.
The next step is to translate this knowledge into better treatments. Instead of searching for one single “anti-aging pill,” researchers envision more targeted therapies.
Someone with genes linked to cognitive frailty might benefit from early interventions to prevent dementia, while another person with metabolic frailty could take steps to avoid diabetes or heart disease.
The ultimate goal, the researchers say, is to develop therapies that address the root causes of aging itself.
While a single pill to stop aging entirely is unlikely, it may one day be possible to have a handful of treatments that target the major pathways of decline, extending not just lifespan, but healthy lifespan.
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