People with a gene variation that blocks a cholesterol-transport protein in the body have a lower risk of developing Alzheimer’s disease, a study found.
Those that had this variation in both copies of the gene, which inhibits the cholesterol ester transfer protein, were about 70 percent less likely to develop Alzheimer’s disease during the study than those without the variation, research in tomorrow’s Journal of the American Medical Association showed.
More than 30 million people worldwide have Alzheimer’s disease, according to the London-based advocacy group Alzheimer’s Disease International. There is no cure yet for the disease, which attacks the brain and causes memory loss. Medicines called CETP inhibitors that mimic the effect of the gene variation in today’s study are under development by Merck & Co. and Roche Holding AG for cholesterol and may prove to work in fighting Alzheimer’s, said study author Richard Lipton.
Today’s findings “may point the way to a new therapeutic avenue for preventing Alzheimer’s disease or promoting successful brain aging,” said Lipton, a professor and vice chairman of neurology at Yeshiva University’s Albert Einstein College of Medicine in Bronx, New York, in a Jan. 8 telephone interview. “These same drugs that have been developed to treat cholesterol may have promise as treatments for Alzheimer’s disease.”
‘Good’ Cholesterol
Those with the gene variation have higher levels of HDL, the high-density lipoprotein or “good” cholesterol in their body. Researchers are unsure what role the variation and higher levels of HDL play in lowering the risk of Alzheimer’s, Lipton said. Researchers looked at data from 523 people from the Einstein Aging Study, which has followed elderly Bronx residents for 25 years. All the participants were cognitively healthy at the start of the study and had their blood analyzed to see if they had a CETP gene variant. They were followed for an average of four years.
During the study, 40 new cases of dementia occurred, most of which were Alzheimer’s disease. The researchers calculated Alzheimer’s disease risk by measuring how long it took people to develop the disease in those with or without the gene variation. They found that those with the variant in both copies of that gene developed Alzheimer’s disease at 30 percent of the rate of those without the variation, Lipton said.
Memory Decline Slowed
The researchers also found that those with the protective gene variation saw their memory decline 51 percent more slowly than those without the variant, he said.
Whitehouse Station, New Jersey-based Merck’s CETP inhibitor anacetrapib and Basel, Switzerland-based Roche’s dalcetrapib are in the last of three phases of testing needed for U.S. Food and Drug Administration approval. Roche plans to seek approval for the treatment in the U.S. after 2012, said Terence Hurley, a Roche spokesman. Lipton said the researchers are studying how CETP acts on the brain to understand its effect on Alzheimer’s and looking for other CETP gene variants that may influence the disease.
By Nicole Ostrow, Jan. 12 (Bloomberg)
