Why some people age faster than others: geneticists have found the answer

Some people keep their minds and bodies vibrant into old age, while others face diabetes, dementia or mobility impairments well into middle age.

A new study led by the University of Colorado at Boulder, published in the journal Nature Genetics, sheds light on the reasons for these differences.

An international team of researchers analysed data from hundreds of thousands of people from the UK Biobank and other bases, identifying more than 400 genes linked to accelerated ageing. This is significantly more than the previously identified 37 genes. This is the first time scientists have linked specific groups of genes to different types of age-related frailty, from cognitive decline to social isolation.

By "frailty," the researchers mean the general physiological decline that accompanies aging. More than 40 per cent of Americans over 65 fall under this definition. The problem is that two people can get the same high frailty index but with different manifestations: one with a clear mind but limited mobility, the other in good physical shape but with impaired memory.

"Aging is not a single disease. There are many manifestations of it," explains one of the study's co-authors, Professor Kenneth Rockwood of Dalhousie University (Canada).

To get to the bottom of which genes are responsible for different forms of age-related disorders, the team conducted a genomic association study, matching DNA data to 30 symptoms of frailty.

Some genes turned out to be particularly important for particular subtypes. For example, SP1, linked to immune function and Alzheimer's disease, turned out to be strongly associated with cognitive decline. And FTO, a gene previously linked to obesity, influenced a range of age-related disorders.

"This study not only clarifies which aspects of aging are different, but also shows that there is a different biology behind each," said lead author Andrew Grotzinger, associate professor of psychology and neuroscience.

The authors suggest that clinical assessments of frailty could be expanded to include six subtypes, allowing for early selection of targeted therapies. For example, a person with signs of cognitive ageing could be offered dementia prevention in advance, while a patient with metabolic frailty could be offered measures to prevent diabetes or cardiovascular disease.

In the future, it is possible that a "polygenic risk" may emerge, where a predisposition to a certain type of ageing can be determined by DNA analysis. The main goal, according to scientists, remains the search for the molecular mechanisms of aging itself - and the creation of drugs that can slow them down.

"It's unlikely we're going to get one magic pill for old age," Grotzinger says. - "But maybe we don't need hundreds - just a few, each targeting specific aspects of aging, will suffice."