The race to turn aging science into medicine

Global life expectancy at birth has doubled since 1900. It’s one of modern medicine’s greatest achievements, and the compounded result of vaccines, clean water, better maternal-child care, and treatments for diseases that would have seemed miraculous a generation ago.

But healthy life expectancy, meaning the years lived free of significant disability or disease, hasn’t kept pace. In many high-income countries, people now spend roughly the last decade of life in meaningful functional decline. We have gotten very good at keeping people alive. We have not gotten as good at keeping them well.

The common driver of that late-life decline is aging itself. Aging underlies the chronic conditions that dominate those years, from heart disease and diabetes to Alzheimer’s. That raises a tantalizing question: If aging drives so many diseases, could targeting the biology of aging help prevent many of them at once?

The life sciences industry is starting to bet that it can.

A widening gap between lifespan and healthspan

The world is getting older. The global population over 60 is projected to double to 2.1 billion by 2050. In the U.S., all 73 million Baby Boomers will have crossed the 65-year threshold by 2030.

Living longer doesn’t mean living healthier. The average American now spends roughly the last 12.5 years of life managing at least one chronic condition, a wider gap than in Japan, South Korea, or much of Western Europe.

For health systems, that’s a major mounting care burden, with fewer working-age people available to provide that care and support its costs. For life sciences companies, it’s a potentially massive commercial opportunity. Unlike a therapy aimed at a single disease, an intervention that targets the biology of aging could have a market that includes virtually everyone.

The science of aging has grown up

In 2013, a landmark paper in Cell introduced the “hallmarks of aging,” a framework describing the molecular and cellular processes that drive biological aging. Since then, the framework has expanded to include 12 hallmarks, spanning processes like cellular senescence, epigenetic changes, and chronic inflammation, among others.

These hallmarks have given drug developers a framework to investigate therapeutic targets that could slow or modify the processes underlying aging. Because these processes are interconnected, influencing one may also affect others, with implications for multiple age-related diseases.

Some of those ideas are now reaching the clinic. In June 2026, Life Biosciences’ ER-100 became the first partial epigenetic reprogramming therapy to enter human trials, targeting optic neuropathies. Partial reprogramming aims to reverse some age-related changes in cells, helping them function more like younger cells while preserving their specialized roles.

Other approaches are advancing, too: senotherapeutics that clear or modulate senescent “zombie” cells, selective mTORC1 inhibitors that build on rapamycin’s strong track record in animal studies, therapies that restore cellular cleanup processes, and efforts to regenerate the aging thymus.

The path hasn’t been smooth. Unity Biotechnology, once a high-profile name in anti-aging research for its approach to clearing senescent cells, saw its lead candidate, UBX1325, reach Phase 2b testing for diabetic macular edema before missing its primary endpoint in 2025, despite gains in visual acuity. The company subsequently wound down operations.

Most current programs remain early-stage. But the breadth of activity shows how aging biology is gaining a foothold in mainstream drug development.

Are GLP-1s the first anti-aging drugs?

Researchers spent decades looking for drugs that could affect aging broadly. GLP-1s may have arrived by accident.

Originally developed for diabetes and later adopted widely for obesity, drugs like Ozempic, Wegovy, and Mounjaro are showing benefits far beyond glucose control and weight loss. The SELECT and FLOW outcome trials showed semaglutide can reduce cardiovascular and kidney events in high-risk patients, and GLP-1s have been associated with lower levels of inflammatory biomarkers. Just as important, they bring something geroscience has long lacked: widely used therapies with extensive human data.

The early aging evidence is intriguing. In a study published in Nature, late-life semaglutide treatment improved physical, metabolic, and cognitive function in elderly female mice and extended median lifespan by nearly 100 days. Notably, treatment began after substantial age-related changes were already underway.

In humans, a post-hoc analysis of a Phase 2b trial in adults with HIV-associated lipohypertrophy, a population with accelerated biological aging, found semaglutide was associated with a 9% reduction in the pace of aging as measured by the DunedinPACE epigenetic clock. Whether those effects extend to broader, healthier populations remains unclear.

The brain is a tougher story. Novo Nordisk’s Phase 3 EVOKE and EVOKE+ trials found that oral semaglutide did not significantly slow Alzheimer’s progression. Still, interest isn’t fading. Definitive Healthcare data shows research activity at the intersection of GLP-1s and dementia and Alzheimer’s disease, including clinical trial starts, publications, and presentations, grew more than 17-fold from 2010 to 2025.

Growth in GLP-1 and dementia/Alzheimer’s research activity, 2010–2025