A gene in the brain of a mouse may hold the key to treating Alzheimer's disease in humans.
Scientists at the Massachusetts Institute of Technology have found a way to slow the loss of memory and learning in mice by working with a gene called SIRT1, which regulates the production of a class of proteins called sirtuin one.
Led by MIT biologist Leonard Guarente, the scientists genetically engineered mice with a type of Alzheimer's disease. They engineered one group to produce more sirtuin one, one group to produce none and left one group as a control.
The researchers found that the mice with the ability to produce extra sirtuin one retained their memory and learning ability as they aged. Mice with Alzheimer's but without the capability to produce extra sirtuin one showed significant declines in learning ability and memory; even worse off were those engineered to produce no sirtuin one.
A neurodegenerative disorder that results in memory loss and impaired cognition, Alzheimer's has been shown to affect one-third of those who reach the age of 80. The cause is thought to be amyloid plaques, which form when proteins are broken down into smaller toxic fragments known as amyloid peptides.
The study shows that sirtuin one can break down the protein into smaller but harmless fragments. Better still, mice with more than one SIRT1 gene showed fewer plaques than mice without it.
SIRT1 has previously been credited for its affect on longevity, which has been found to activate under a calorie-restricted diet or with red wine, by the compound resveratrol.
But SIRT1's connection to Alzheimer's is a big deal, since years of research has yielded little insight into how to treat the illness. (A recent study by Guarente's MIT colleague Li-Huei Tsai also hinted at the affect of sirtuins on memory apart from disease.)
There are still questions. It's unclear whether mice are a good model for Alzheimer's disease in humans, and even if so, a drug to boost SIRT1 levels must get past the blood-brain barrier to reach brain cells -- a challenge even for drug giant GlaxoSmithKline, which is working on a solution.
Co-authored by Gizem Donmez, Dena Cohen and Diana Wang, the study was published in the July 23 issue of the journal Cell.
It was funded by the American Parkinson Disease Association, the National Institutes of Health and the Paul F. Glenn Foundation.
Photo: Donna Coveney/MIT
This post was originally published on Smartplanet.com