Alzheimer’s disease is the leading cause of dementia and the sixth leading cause of death in the U.S. The disease has both genetic and environmental risk factors, and up to a third of cases may be the result of modifiable lifestyle influences such as a diet high in saturated fat and sugar.
Individual genetic variation affects how environmental risk factors may raise or lower a person’s risk for Alzheimer’s disease, but these gene-by-environment interactions are poorly understood.
The Alzheimer’s Association has awarded a three-year research fellowship totaling $174,973 to , a postdoctoral associate in the laboratory of Jackson Laboratory (JAX) Associate Professor , for her studies of how genetics and diet interact to determine risk for Alzheimer’s disease.
Gene-by-environment interactions are difficult to study in humans, Dunn notes, because clinical studies are inconsistent in their reporting of modifiable risk factors such as diet. Traditional mouse models of Alzheimer’s disease have no genetic variation, and therefore are also poorly suited for understanding the effects of diet on a genetically varied population.
“To overcome these barriers,” Dunn explains, “we developed a mouse model of Alzheimer’s disease with a portion of the genetic variability observed in humans, allowing us to study complex genetic and environmental contributors to the disease.”
These studies, she says, “have the potential to identify new therapeutic targets for Alzheimer’s disease, in addition to enhancing our ability to develop personalized treatment strategies based on a person’s genetic and environmental risk factor profile.”