In elderly mice barely able to climb a treadmill, scientists at the University at Buffalo made a startling discovery: by stabilizing a single protein called tristetraprolin, the animals regained strength, built healthier bones, and moved with noticeably improved vigor. The findings, published in January 2026, offer a glimpse into how aging might one day be slowed in humans—not through expensive interventions, but by manipulating the body's own molecular machinery.
The research tackles a phenomenon scientists call "inflammaging": a constant, low-level state of inflammation that gradually damages tissues and weakens the aging body. As Keith Kirkwood, senior associate dean for research at UB's School of Dental Medicine, explains, this age-related immune decline—known as immunosenescence—leaves older people vulnerable to chronic inflammatory diseases, weakened immunity, bone loss, and declining strength. With nearly one in four Americans expected to be age 65 or older by 2050, many living well into their 90s, understanding what drives these changes has become urgent.
Kirkwood's team focused on tristetraprolin (TTP), an RNA binding protein that acts like a cleanup crew for the immune system. It breaks down inflammatory signals before they accumulate and damage the body. Here's the catch: as people age, TTP levels naturally plummet, especially in immune cells. That drop allows inflammation to spread more widely throughout the body. The researchers hypothesized that restoring TTP could reverse some aging-related health problems.
To test the theory, the team genetically modified a group of elderly mice—22 months old, which counts as elderly in mouse years—so that TTP remained stable instead of declining. Over six years, supported by a $2.1 million grant from the National Institutes of Health, they evaluated the animals using grip strength, walking speed, treadmill endurance, and overall energy levels.
The results were striking. Male mice with increased TTP levels showed significantly lower frailty scores than untreated mice. They demonstrated better grip strength, faster walking, improved endurance, and more youthful-looking immune profiles. Their bones were notably healthier, with reduced bone breakdown. Female mice also improved, though the changes were smaller—possibly because of their smaller body size and declining estrogen levels, which may limit how tissues respond to anti-inflammatory changes. Yet even the female mice developed stronger bones when TTP expression was enhanced.
The practical implications are profound. In the United States, about 15 percent of non-nursing home adults aged 65 and older experience frailty. Understanding the connections between inflammaging, immune changes, bone health, and frailty could eventually lead to targeted interventions that improve quality of life for aging populations.
Still, Kirkwood urges caution. Human treatments remain far away. Collaborators including Perry Blackshear, a retired investigator formerly affiliated with Duke University and the National Institute of Environmental Health Science, have begun screening compounds that might increase TTP expression in humans, but none have yet produced clear success. The team is now planning additional studies to explore whether TTP could also reduce neuroinflammation linked to aging disorders like dementia and Alzheimer's disease.
For now, the elderly mice climbing their treadmills represent a proof of concept—evidence that manipulating a single protein might one day help humans age with more strength and vitality.