Aging Research

What is aging research?

Aging research, also called geroscience, starts from a simple observation: heart disease, cancer, Alzheimer's, and diabetes all become dramatically more common after age 50. Instead of treating each disease separately, geroscience asks what drives them all. The answer is aging itself. If you can slow the biological processes behind aging, you reduce the risk of every age-related disease at once.

This isn't a fringe idea anymore. The National Institute on Aging funds geroscience as a core research program. A 2025 Cell paper by Guido Kroemer and colleagues formalized the concept of "precision geromedicine," proposing that aging can be managed through targeted interventions the same way oncology targets cancer mutations ^[1]. The field has moved from theoretical to clinical in under a decade.

The 12 hallmarks of aging

In 2013, Carlos Lopez-Otin and colleagues published a framework of nine hallmarks of aging in Cell. The 2023 update expanded this to twelve ^[2]. These hallmarks include genomic instability, telomere shortening, epigenetic drift, loss of proteostasis (protein quality control), deregulated nutrient sensing through mTOR and AMPK pathways, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. The three new additions are disabled macroautophagy (the cell's recycling system), chronic low-grade inflammation (often called "inflammaging"), and gut microbiome dysbiosis.

What makes the hallmarks framework so useful is that each hallmark is a potential drug target. Rapamycin inhibits mTOR. Senolytics clear senescent cells. NAD+ precursors address mitochondrial decline. The framework turned aging from an abstract concept into a list of actionable biological problems.

Therapies in clinical testing

Senolytics

Senescent cells stop dividing but refuse to die. They accumulate with age and pump out inflammatory signals called the SASP (senescence-associated secretory phenotype). The combination of dasatinib and quercetin (D+Q), developed by James Kirkland's group at Mayo Clinic, selectively kills these cells. A 2025 pilot study in eBioMedicine tested D+Q in older adults with mild cognitive impairment and slow gait speed, and found it was safe and feasible over 12 weeks ^[3]. An earlier trial in idiopathic pulmonary fibrosis showed reduced senescent cell markers ^[4]. Fisetin, a plant flavonoid, is being tested as a gentler alternative.

Metformin and the TAME trial

The TAME trial (Targeting Aging with Metformin) is the first clinical trial designed to treat aging as a medical condition. It plans to enroll 3,000 adults aged 65 to 79 and track whether 1,500 mg/day of metformin delays the onset of multiple age-related diseases over four years. After years of funding delays, the trial is now being organized through ARPA-H ^[5]. Meanwhile, a 2024 study in Signal Transduction and Targeted Therapy showed that metformin slowed epigenetic aging clocks in cynomolgus monkeys over 3.3 years ^[6]. The evidence is growing, but human proof is still pending.

Rapamycin

Rapamycin inhibits mTOR, a nutrient-sensing pathway linked to aging in virtually every organism studied. The PEARL trial, published in 2025, followed 114 healthy adults taking 5 or 10 mg weekly rapamycin for one year. It was well tolerated and produced modest changes in biological aging biomarkers, though clinical benefits remain unproven in long-term studies ^[7]. A separate 2025 Oxford study found that low-dose rapamycin reduced senescent cell counts in older adults.

Epigenetic reprogramming

Partial cellular reprogramming using Yamanaka factors (Oct4, Sox2, Klf4) is the most ambitious approach in aging research. A 2024 study showed that gene therapy delivering these factors to old mice extended their remaining lifespan by 109% and reversed epigenetic age markers ^[8]. Life Biosciences plans to bring its reprogramming therapy ER-100 into human clinical trials for optic neuropathies in 2026. The risk is real: too much reprogramming can trigger tumor formation. But the potential to actually reverse aging, not just slow it, makes this the frontier to watch.

What aging research means for you today

Most anti-aging drugs are still experimental. But the research has confirmed what works right now: regular exercise reduces biological age by multiple epigenetic clocks. Sleeping 7 to 8 hours nightly cuts all-cause mortality risk by up to 30%. A Mediterranean-style diet lowers inflammatory biomarkers. Caloric restriction, even modest 10 to 15% reductions, is the most replicated longevity intervention in animal models. These aren't consolation prizes while we wait for drugs. They're the strongest interventions we have, and emerging therapies will likely work best on top of them.