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2016 Grants - Hohsfield
Manipulating Microglia to Prevent Alzheimer’s Disease
Lindsay Hohsfield, Ph.D.
University of California, Irvine
2016 Alzheimer’s Association Research Fellowship (AARF)
Can regulating the function of microglia in the brain help reduce inflammation associated with Alzheimer’s disease?
One of the characteristic features of Alzheimer’s disease is inflammation in the brain. Inflammation is controlled by the immune system, and the primary immune cells in the brain are known as microglia. Inflammation is the normal response of the body to infection or injury and is turned off after the condition is resolved. In Alzheimer’s disease, however, inflammation in the brain remains high, possibly contributing to disease progression. Microglia are important for clearing toxic proteins such as beta-amyloid and abnormal tau from the brain, but when microglia become overactivated during Alzheimer’s disease, this function may be impaired.
Lindsay Hohsfield, Ph.D., and colleagues have found that during Alzheimer’s disease microglia appear to become chronically overactivated. In initial studies using Alzheimer’s-like mice, they used a drug that depletes the brain of overactived microglia. When the drug is removed, new microglia are generated that appear to have more neuroprotective properties. They will repeat this method for their current studies and determine if it can help prevent brain changes associated with Alzheimer’s disease. They will measure brain inflammation, levels of beta-amyloid and tau, and memory abilities in the mice. They will also identify which genes and proteins may be involved in the control of microglia function.
This research could shed new light on the role of microglia in Alzheimer’s disease and explore the effectiveness of a potential treatment to reduce inflammation in the brain. These findings could inform the development of novel therapies that regulate microglia function to help slow or prevent disease progression.