5th edition 2027

GLP-1 drug semaglutide extends lifespan and slows ageing in older mice

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A new study suggests that the GLP-1 drug semaglutide may slow certain aspects of biological aging and potentially extend lifespan. Funded by the National Institutes of Health (NIH), the research was conducted in older, healthy mice at the University of California, Berkeley.

Researchers found that three months of semaglutide treatment improved muscle and cognitive performance in older female mice while reducing several biological markers linked to aging. In a separate group monitored throughout their lives, mice treated with semaglutide had a median lifespan nearly 100 days longer than untreated animals.

The findings add to growing evidence that GLP-1 drugs may influence the aging process itself rather than simply reducing the risk or severity of individual age-related diseases. Researchers noted that because many chronic diseases are closely connected to aging, slowing biological aging could potentially produce broader health benefits.

Led by Danica Chen, Professor of Metabolic Biology and Nutrition at UC Berkeley, the researchers treated 20-month-old female mice with semaglutide for three months. Compared with untreated animals, the treated mice demonstrated improvements in measures of muscle and cognitive function. Gene-expression analysis also showed reductions in several features associated with natural aging, including inflammation and reduced regenerative capacity.

The team then examined whether these effects were primarily caused by semaglutide's ability to reduce food intake. Another group of 20-month-old female mice followed a calorie-restricted diet for five months, with their food intake designed to resemble that of the semaglutide-treated animals.

The researchers observed considerable similarities between the two groups across many physiological measures. However, semaglutide-treated mice showed improvements beyond baseline levels in exploratory activity, spatial memory, and blood-glucose regulation. Metabolic rate also differed between the groups, declining in calorie-restricted mice while remaining relatively stable in those receiving semaglutide.

These differences suggest that semaglutide may influence certain biological pathways independently of calorie restriction. According to the researchers, identifying these mechanisms could help advance the development of future interventions aimed at promoting healthy aging and longevity.

The researchers emphasized that the findings are based on animal studies and cannot yet be directly applied to humans. Further clinical research is needed to determine whether GLP-1 drugs can slow biological aging or extend healthy lifespan in people. Future studies may also explore their potential benefits in healthy older adults beyond their current use for metabolic and age-related conditions.

Source: https://www.drugtargetreview.com/glp-1-drug-semaglutide-extends-lifespan-and-slows-ageing-in-older-mice/2136393.article