Eight years ago I wrote an article about particles. More precisely, I wrote about how, when it comes to lipoprotein particles like the notorious LDL and the vaunted HDL, the bigger and fluffier the better from a health standpoint. In the course of researching the article I telephoned Nir Barzilai, MD, of Yeshiva University's Albert Einstein College of Medicine.
Barzilai has assembled a collection of over 500 Ashkenazi Jews 95 years old or older, leveraging this relatively homogeneous group to tease out gene variants that distinguish long-lived from shorter-lived but otherwise similar people. Among the interesting longevity-associated gene variants he's fished out is one whose presence renders HDL and LDL particles larger and more bouyant. (Think of this as the biochemical equivalent of dotting I's with big round circles, which connotes an optimistic outlook.)
I finally got to meet Barzilai in person at a symposium (read about it here) hosted by the Glenn Laboratories for the Biology of Aging. Directed by Tom Rando, MD, PhD, this Stanford-based center focuses on how changes in stem cells in various tissues that occur as we get older contribute to the development of age-related disorders.
The Jan. 30 event was the kickoff for an ongoing series of Monday-afternoon seminars that will highlight advances in our understanding, at a fundamental level, of the aging process.
A key point that Barzilai, Rando and other symposium speakers broadly agreed on: Like tots engaged in parallel play in a sandbox, investigators have tended to focus narrowly on one or another of numerous aging-related diseases from cancer to arthritis to Alzheimer's, without necessarily talking to one another very much. But slowing the aging process, the speakers emphasized, will delay or prevent all those diseases.
Sign me up for that plan.