A team led by researchers at the School of Medicine has identified variations in a gene that double a person’s risk of developing Alzheimer’s disease later in life. Pictured are Carlos Cruchaga, PhD (left), and Alison M. Goate, DPhil, who led the research effort.
Studying spinal fluid from people at risk for Alzheimer’s disease, School of Medicine researchers have found that a gene variation that had not been considered risky actually can increase the chances of developing Alzheimer’s disease when it occurs in tandem with another gene variant known to elevate risk. Shown is an image of a brain with a buildup of amyloid deposits (highest amounts in yellow and red) that collect to form senile plaques in patients with Alzheimer’s.
Scientists’ picture of how a gene strongly linked to Alzheimer’s disease harms the brain may have to be revised, researchers at the School of Medicine have found. Washington University’s David M. Holtzman, MD, says leading researchers recently agreed that targeting this gene is a promising approach for gaining a better understanding of and improving treatments for the disease.
Researchers at Washington University have identified a new set of genetic markers for Alzheimer’s disease that point to a second pathway through which the disease develops. Much of the genetic research in Alzheimer’s centers on amyloid-beta, a key component of brain plaques in people with the disease. But the new study identified several genes linked to the tau protein, which is found in tangles.
The same gene mutations linked to inherited, early-onset Alzheimer’s disease have been found in people with the more common late-onset form of the illness. The discovery by researchers at Washington University School of Medicine in St. Louis may lead doctors and researchers to change the way Alzheimer’s disease is classified.
Scientists at Washington University School of Medicine in St. Louis have found that a protein made by a key Alzheimer’s gene slows the brain’s ability to get rid of amyloid beta, the main ingredient of the amyloid plaques that characterize the devastating illness.