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2023 Alzheimer's Association Research Fellowship to Promote Diversity (AARF-D)

Biased GPR3 signaling mediates glial activation in Alzheimer's Disease.

Can loss of a specific protein in the brain change how cells function in Alzheimer’s?

Roberta Reis, Ph.D.
University of Pittsburgh
Pittsburgh, PA - United States


Two of the hallmark brain changes in Alzheimer’s are the accumulation of beta amyloid and tau which form plaques and tangles, respectively. The formation of beta-amyloid plaques negatively impacts several types of cells in the brain, contributing to cognitive decline and Alzheimer’s. Recent studies have shown that glial cells, such as astrocytes (the “support cells” of the nervous system) and microglia (the primary immune cells of the brain) play a role in removing plaques in the early stages of Alzheimer’s. However, the precise mechanisms are unknown. 

In initial studies, Dr. Roberta Reis and colleagues identified a specific protein called GPR3 (G-protein coupled receptor 3) that may be protective against cognitive decline by helping the glial cells remove plaques.

Research Plan

Building on their initial findings, Dr. Reis and team will investigate how GPR3 impacts glial cell function in Alzheimer’s. They will test whether reducing GPR3 levels in genetically-engineered Alzheimer’s like mice impacts astrocyte and microglia function, as well as investigate whether reducing GPR3 impacts plaque accumulation. Next, the researchers will use astrocytes and microglia grown in a laboratory dish that have either high or low levels of GPR3 to understand the mechanisms by which GPR3 impacts glial cell function.


If successful, the results of this study may shed new light on the mechanisms that impact plaque accumulation. It could also lead to novel methods of reducing plaque levels and protecting cognitive health in individuals with Alzheimer’s.

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