More than 90% of adults over 65 have at least one chronic condition and about 80% have two or more, according to the Centers for Disease Control and Prevention.
Rather than simply treating ailments individually, researchers are exploring new pathways with pharmaceuticals originally designed for different purposes, targeting the cellular, metabolic and molecular drivers of aging itself.
A five-year, $22 million study being undertaken by a national research consortium led by Brown University and the University of Rochester aims to investigate whether a drug initially used to treat HIV might also play a role in extending human life.
The team, led by biology professor John Sedivy, director of Brown’s Center on the Biology of Aging, and Vera Gorbunova, co-director of the Rochester Aging Research Center and professor of biology at the University of Rochester, hypothesize that moderating the activity of these genetic elements with drugs such as censavudine – originally designed to treat HIV – could mitigate chronic inflammation commonly associated with aging.
Since the drug inhibits “reverse transcriptase,” the enzyme that retrotransposons need to replicate, the theory is retrotransposon activity may be suppressed, reducing the chronic inflammation triggered by DNA that drives much of age-related decline.
Sedivy said that the use of HIV drugs is practical because of the genetic connections between retrotransposons and the HIV virus.
“What’s new and really exciting about this project is that the goal is not to treat diseases but to treat aging itself,” Sedivy said. “This project will launch a large, credible clinical trial with healthy older people to see if a drug can slow the human aging process.”
The randomized, placebo-controlled study trial focuses on LINE-1 retrotransposons, virus-like sequences often called “selfish” genes, “junk DNA,” or “molecular parasites“ that make up a large portion of the human genome and are notorious for their role in amplifying a “false alarm” within the immune system that typically recognizes them as viral threats, prompting an immune response that can lead to severe inflammation.
As people age, these genes become increasingly active, contributing to inflammation and increasing the odds of age-related diseases such as Alzheimer’s disease and amyotrophic lateral sclerosis, or ALS.
The study plans to enroll around 200 healthy participants age 60 to 65 who will receive either the drug or a placebo over a 48-week period. Brown is receiving approximately $2 million for the clinical trials.
In addition to Transposon Therapeutics, a biotech startup founded on intellectual property licensed from Brown, other collaborating institutions include the University of Connecticut and the University of Texas Medical Branch.
The project is funded by the federal Advanced Research Projects Agency for Health, created to find “high-risk, high-reward” strategies to address long-term public health.
In announcing the funding, ARPA-H Director Alicia Jackson said in a statement that “defeating chronic, debilitating diseases will not just take new therapies but novel and evidence-based prevention approaches.”
The Brown funding came from an ARPA-H initiative called Proactive Solutions for Prolonging Resilience – or PROSPR – that seeks to extend “healthspan,” the number of years a person lives in good health.
Transposon chairman and CEO Dennis Podlesakcalled the funding “a transformative opportunity to advance [Censavudine] into an entirely new therapeutic category that targets the underlying causes of age-related disease.” He added, “with no [Food and Drug Administration-approved] therapies to extend healthspan, we believe [censavudine] has the potential to be at the forefront with a first-in-class approach to preserving function, preventing long-term disease and extending the years of healthy life.”
In Rhode Island, 18% of the state is now 65 or older. And in 2025, the state had the highest rates for high cholesterol, hypertension, and having four or more chronic conditions among all New England states, according to the state’s annual Aging Report.
Chronic inflammation, while a major contributor to aging, is influenced not only by the deactivation of retrotransposons but also by various other cellular failures and dysfunctions, such as an increase in senescent cells or mitochondrial dysfunction, said Giuseppe Coppotelli, research assistant professor at the Department of Biomedical and Pharmaceutical Sciences at the University of Rhode Island.
“Its causes are not related to a single process but rather several,” he said.
Aging has been successfully slowed down in model organisms and even in primates, but the challenge remains in translating findings into effective human therapies.
“The ultimate success would provide a way to restore order in the cells and forestall at least some of the molecular ravages of age,” Sedivy said.
