It’s something we’ve all noticed: some people seem to grow old gracefully, while others face serious health problems much earlier in life.
One person may stay sharp and active well into their 90s, while another may start struggling with diabetes, Alzheimer’s disease, or walking difficulties decades earlier. Some can recover quickly from a fall or the flu, while others never regain their health.
A new international study led by researchers at the University of Colorado Boulder has taken a big step toward understanding why this happens.
The findings, published in the journal Nature Genetics, reveal more than 400 genes linked to what scientists call “accelerated aging” or “frailty.” These genes seem to play different roles in different types of age-related decline, from memory loss to weak muscles to even social isolation.
This discovery supports an idea known as the “geroscience hypothesis.” Instead of trying to treat each age-related disease separately—like heart disease, diabetes, or dementia—the hypothesis suggests that doctors should focus on treating the process of aging itself.
If aging can be slowed or managed, then many diseases that come with age might also be delayed or reduced.
Frailty is a medical term doctors use to describe the overall decline in physical and mental health that often happens with aging. In the United States, more than 40% of adults over the age of 65 are considered frail.
Doctors usually measure frailty with a 30-point checklist that includes things like walking speed, grip strength, the number of illnesses, and how socially active someone is.
But this test has a problem: two people could score equally high on frailty while being completely different. One person may be physically strong but losing memory, while another may be sharp-minded but unable to walk.
This lack of detail has made it hard for doctors to give useful advice and for scientists to identify what exactly drives unhealthy aging. As Dr. Kenneth Rockwood, a frailty expert from Dalhousie University in Canada and co-author of the study, put it: “Aging is not just one thing. There are many ways to be frail. The question is, what genes are involved?”
To answer this, the team studied genetic and health data from hundreds of thousands of people in the UK Biobank and other public datasets. They searched for connections between DNA and 30 frailty symptoms. They ended up identifying 408 genes connected to aging-related decline—far more than the 37 genes that had previously been found.
Even more interesting, different sets of genes appeared to be linked to different types of unhealthy aging. For example, the gene SP1, which is connected to immune function and Alzheimer’s disease, was strongly associated with poor memory and thinking skills.
Meanwhile, the FTO gene, already known for its role in obesity, was tied to several categories of unhealthy aging.
The researchers grouped these findings into six “subtypes” of frailty: disability, poor cognition, metabolic problems, multiple diseases, unhealthy lifestyle, and limited social support. Each subtype appears to have its own biological pathway, which means different people may age in different ways depending on their genetics.
So what does this mean for the future? The researchers suggest that doctors may one day test patients not only for general frailty but also for these six subtypes. This could help guide more targeted prevention.
For instance, someone showing signs of cognitive frailty could start brain-focused therapies early, while someone with metabolic frailty could take steps to prevent diabetes or heart disease.
Lead author Isabelle Foote, a postdoctoral researcher at CU Boulder, hopes that in the future people could get a genetic test, sometimes called a “polygenic risk score,” to learn which type of frailty they are most at risk for.
Even more ambitious is the long-term goal: finding the molecular pathways that actually drive aging and developing treatments to slow them down.
Does this mean a single anti-aging pill is around the corner? Probably not. But senior author Andrew Grotzinger suggests that it may one day be possible to have a few treatments targeting groups of age-related problems—like one pill for metabolic issues and another for cognitive decline—rather than hundreds of separate medications for each condition.
This research does not promise a magic cure, but it brings us closer to understanding why aging looks so different from person to person. By learning which genes control different forms of frailty, scientists may one day be able to design personalized treatments that help people stay healthier and more independent for longer.
The study is groundbreaking because it shifts the conversation from treating individual diseases to targeting the root process of aging. It confirms that aging is not one uniform process but a collection of different pathways, each influenced by different genes.
This means future therapies will likely need to be personalized, focusing on a person’s unique genetic risks. The research also suggests that genetic testing could one day become a standard part of aging care, giving people insights into how they are likely to age and what steps they can take to protect themselves.
While a single pill for aging is unlikely, a small number of targeted treatments could transform how society manages age-related diseases.
If you care about Alzheimer’s disease, please read studies about Scientists find a new way to treat Alzheimer’s disease and findings of Fluctuating cholesterol and triglyceride levels are linked to Alzheimer’s disease.
For more about Alzheimer’s disease, please read studies about Scientists find root cause of tau tangles in Alzheimer’s disease and findings of new treatment for early-onset Alzheimer’s disease.
The study is published in Nature Genetics.
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