It is well established that there is elevated inflammation in Alzheimer’s disease, while hippocampal neurogenesis (a type of brain plasticity) is decreased in the brains of Alzheimer’s patients. Research has shown that gut microbiota may be a master regulator of both inflammation and neurogenesis, and emerging research suggests a key role of the microbiota-gut-brain axis in Alzheimer’s development. Thus, targeting the microbiota may be a new avenue to develop knowledge for Alzheimer’s treatment.

Exercise promotes neurogenesis and may prevent cognitive decline with age. Gut-microbiota composition and related metabolites can also be changed by exercise to confer benefits on brain health. However, the mechanism(s) underlying these effects is not well understood. We hypothesize that the gut-microbiota regulates the effects of exercise on cognition in Alzheimer’s, through changes in inflammation, amyloid plaque pathology and neurogenesis. Our main objective is to develop new strategies for managing memory impairments in Alzheimer’s by investigating if exercise modulates behavior and pathology through the microbiota-gut-brain axis (a bidirectional communication link between our gut microbes and the brain). In this project we will a) determine if exercise can reduce the development of memory impairments and neuropathology in a mouse model of Alzheimer’s, and b) determine if the beneficial effects of exercise can be transferred from mice-to-mice via gut-microbial-mediated mechanisms. This project will contribute novel knowledge of exercise as a preventative/therapeutic strategy for Alzheimer’s.