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.
Biologists Vera Gorbunova and Andei Seluanov have discovered one reason for the the increase in DNA damage as we age: the primary repair process begins to fail and is replaced by one that is less accurate.
A $9.5 million grant from the National Institute on Aging will support research into the factors responsible for longevity in various species of long-lived rodents, with the goal of developing treatments to improve the aging process in people.