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2017 Grants - Aguilar
Elucidating the Therapeutic Potential of Intersectin in Alzheimer's Disease
Byron J. Aguilar, Ph.D.
East Carolina University
Greenville, North Carolina
2017 Alzheimer’s Association Research Fellowship to Promote Diversity (AARF-D)
Can a molecule that helps coordinate multiple cellular processes disrupted in Alzheimer’s be a target for future therapies?
Chief hallmarks of Alzheimer’s disease include the clumping of toxic beta-amyloid and tau protein into amyloid plaques and tau tangles. Scientists, however, are beginning to understand the role that other molecules play in the disease. One of these molecules is intersectin, it is known to interact with mitogen-activated protein kinase (MAPK), a protein linked to inflammation, and cell division cycle 42 (CDC42), a protein involved in cell division. Studies indicate that intersectin becomes dysfunctional in Alzheimer’s, possibly affecting the other biochemical pathways, such as MAPK and CDC42 activity as well.
In preliminary studies, Byron J. Aguilar, Ph.D., and colleagues have developed compounds that can prevent intersectin from interacting with MAPK and CDC42, which could block problems with inflammation and cell division.
For their current grant, Dr. Aguilar and his team will study how intersectin inhibitors hinder intersectin/MAPK and intersectin/CDC42 activity in Alzheimer’s. Their project will involve mice genetically engineered to develop Alzheimer’s-like brain changes. The researchers will administer intersectin inhibitors to their mice. They will then examine the rodents’ brains to identify mechanisms that underlie the intersectin inhibitors beneficial effects on inflammation and cell cycle processes. They will also look to clarify exactly how intersectin becomes dysfunctional in the mice.
The results of this project will shed new light on the role of intersectin in Alzheimer’s disease. They could also identify intersectin inhibitors as part of a novel strategy for treating the disorder.