Anti-Aging-Medizin hat gerade 371 völlig neue genetische Ziele gewonnen | Wissenschaftler haben die detaillierteste genetische Blaupause von Gebrechlichkeit abgebildet und bieten neue Hoffnung auf die Entwicklung wirksamer Anti-Aging-Therapien.

From the article: In a groundbreaking study, scientists have mapped the most detailed genetic blueprint yet of frailty – the age-related decline in resilience that affects around 40% of people aged 65 and above, dramatically increasing the risk of hospitalization, disability and death. The findings offer new hope in the development of effective anti-aging therapies.

In the largest [study](https://www.nature.com/articles/s41588-025-02269-0) of its kind, University of Colorado Boulder (CU Boulder) researchers led an international team that analyzed the DNA of more than 400,000 people, focusing on six key areas of frailty: physical strength, mobility, cognition, mood, cardiovascular health and nutritional status. Together, they paint a clear picture of how our bodies lose resilience over time – and some faster than others.

„Aging is not just one thing,“ said the study’s co-author Dr. Kenneth Rockwood, a leading expert in frailty, based at Dalhousie University in Nova Scotia. „There are many ways to be frail. The question then becomes: What genes are involved?“

Using a combination of genetic tools – genome-wide association studies (GWAS) and genomic structural equation modeling (gSEM) – the team scanned millions of DNA markers to find variants linked not just to one symptom at a time, but to the overlapping biology that underlies multiple frailty traits. This approach uncovered 408 genetic loci (regions on the genome) associated with frailty – 371 of these had never before been linked to aging.

Many of the signals clustered in biological pathways are already suspected in contributing to advanced aging: chronic inflammation, metabolism, cardiovascular health and brain function. Others overlapped with known risk genes for Alzheimer’s disease, type 2 diabetes, depression and obesity, strengthening the idea that frailty is not a single condition but a web of interrelated processes.

An example the researchers give is the SP1 gene, which is associated with immune function and Alzheimer’s disease. They found it was strongly associated with the broad “poor cognition” subtype; while the FTO gene, associated with obesity, seemed to underlie several different subtypes. While it sounds a little confusing, that’s because it is – it’s a complex tangle of biological influences, which show that frailty is anything but a catch-all sign of aging.

„What this paper does is not only identify sub-facets of disordered aging but also demonstrate that there is very different biology underlying them,“ said senior author Andrew Grotzinger, assistant professor of psychology and neuroscience at CU Boulder. „The tangible next step is to figure out how to treat this underlying biology.“