Aging

Rochester scientists discover that long-lived bats resist cancer thanks to strong immune systems and protective genes—findings that could offer new insights into human aging and disease prevention.

Bats carry many viruses, including the one behind COVID-19, without becoming ill. University of Rochester biologists are studying the immune system of bats to find potential ways to "mimic" that system in humans.

Now in its fifth year, the d.health Summit will address the non-medical factors the affect health, such as economic security, education, physical environment, employment, social support networks, and access to care.

Research from Rochester biologists shows that a class of genomic parasites may cause more harm than previously thought, triggering inflammation that causes age-related diseases.

Rochester biologists were surprised to see that despite its remarkable longevity, the naked mole rat still has cells that undergo senescence, like the cells in much shorter-lived mice.

Nearly one-fifth of the U.S. population will be 65 or older by the year 2030. To address this challenge, the University's third annual d.health Summit will convene thought leaders across health care, finance, technology, and policy.

There are many examples of DNA damage being associated with aging, but never has a reduction in DNA damage been shown to extend lifespan. Rochester research has made this connection, and identified an enzyme that can be targeted to reduce that damage.

Underpinning this year’s theme are a selection of topics that discuss the future of medicine, technology, and healthcare policy as they relate to aging Americans. This national forum will be held at The New York Academy of Sciences, at the World Trade Center in New York City.

Researchers who specialize in the study of aging have identified a protein that may serve as a first responder, activating a “longevity gene” known as sirtuin 6 and setting in motion a cascade of molecular first responders to repair damaged DNA.

Biology researchers Vera Gorbunova and Andrei Seluanov report that the “jumping genes” in mice become active as the mice age when a multi-function protein stops keeping them in check in order to take on another role. A protein called Sirt6 is needed to keep the jumping genes—technically known as retrotransposons—inactive.