The role of GPR37 in Alzheimer's disease pathogenesis
A hallmark of Alzheimer’s disease (AD) is the accumulation of amyloid beta (Aβ) plaques in the brain. In response to Aβ accumulation, other cells in the brain (astrocytes and microglia) undergo molecular, morphological, and functional changes. Healthy astrocytes have the ability to clear Aβ, but the plaque-associated astrocytes cannot. In the proposed research, Dr. Sharon Owino will study how astrocytes change and respond to signals during the development of AD. Dr. Owino will use a mouse model of AD, which is missing a key receptor called GPR37. This will allow her to compare the severity and progression of AD in mice with and without this receptor to better understand its function in disease progression.
