LONGEVITY GENE

ScienceDaily (Jan. 13, 2010) — Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease.
The paper describing the Einstein study is published in the January 13 edition of the Journal of the American Medical Association.

"Most work on the genetics of Alzheimer's disease has focused on factors that increase the danger," said Richard B. Lipton, M.D., the Lotti and Bernard Benson Faculty Scholar in Alzheimer's Disease and professor and vice chair in the Saul R. Korey Department of Neurology at Einstein and senior author of the paper. As an example, he cites APOE ε4, a gene variant involved in cholesterol metabolism that is known to increase the risk of Alzheimer's among those who carry it.

"We reversed this approach," says Dr. Lipton, "and instead focused on a genetic factor that protects against age-related illnesses, including both memory decline and Alzheimer's disease."

In a 2003 study, Dr. Lipton and his colleagues identified the cholesteryl ester transfer protein (CETP) gene variant as a "longevity gene" in a population of Ashkenazi Jews. The favorable CETP gene variant increases blood levels of high-density lipoprotein (HDL) -- the so-called good cholesterol -- and also results in larger-than-average HDL and low-density lipoprotein (LDL) particles."

"We found that people with two copies of the longevity variant of CETP had slower memory decline and a lower risk for developing dementia and Alzheimer's disease," says Amy E. Sanders, M.D., assistant professor in the Saul R. Korey Department of Neurology at Einstein and lead author of the paper. "More specifically, those participants who carried two copies of the favorable CETP variant had a 70 percent reduction in their risk for developing Alzheimer's disease compared with participants who carried no copies of this gene variant."

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