'Longevity' Gene May Cut Dementia Risk
Study Shows CETP Gene May Prevent Age-Related Cognitive Decline
Jan. 12, 2010 -- The so-called "longevity gene" may do more than add years to your life. It may also help stave off age-related cognitive decline, and this discovery is paving the way for new drugs to treat Alzheimer's disease, a study shows.
The longevity gene is a variant of the cholesteryl ester transfer protein (CETP) gene, which was discovered in 2003. This variant has been shown to improve cholesterol levels by increasing HDL "good" cholesterol and regulating the size of cholesterol particles. As a result, it has been linked to longevity and lower heart disease risk, but how or if this variant affects the cognitive decline that is known to occur with aging was not known -- until now.
The study is published in the Jan. 13 issue of the Journal of the American Medical Association.
Researchers analyzed the blood of 523 people aged 70 and older with no signs of cognitive decline to see which copy or copies of the CETP gene they carried. People in the study also underwent standard neuropsychological and neurological testing each year from 1994 to 2009 and performed tests to measure memory, attention span, and the time it takes to process and react to a signal (psychomotor speed).
During 4.3 years of follow-up, there were 40 new cases of dementia seen among this group. Those participants who had a specific variation of the CETP gene were less likely to experience a decline in memory and to develop dementia.
"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 study researcher Amy E. Sanders, MD, assistant professor in the Saul R. Korey Department of Neurology at the Albert Einstein College of Medicine in the Bronx, N.Y., in a news release.
"More specifically," she says, "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."
This variant alters the gene so that the protein it encodes for will functions less efficiently than usual, the researchers explain. Now, drugs are now being developed that mimic this effect.
"These agents should be tested for their ability to promote successful aging and prevent Alzheimer's disease," says study researcher Richard B. Lipton, MD, the Lotti and Bernard Benson Faculty Scholar in Alzheimer's Disease and professor and vice chairman in the Saul R. Korey Department of Neurology at Albert Einstein College of Medicine, in a news release.