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2014 Grants - Brady
Signaling Pathways, Molecular Motors and Cell Specificity in Alzheimer’s Disease
Scott Brady, Ph.D.
University of Illinois — Chicago
2014 Zenith Fellows Award
In Alzheimer’s disease and some other degenerative disorders of the brain, certain types of brain cells are selectively vulnerable to cell death, and the types of cells that are vulnerable are specific to each disease. Scientists do not fully understand why certain brain cells are especially vulnerable in Alzheimer’s disease, but such understanding could lead to new strategies to halt or slow disease progression.
The brain cell types that appear particularly vulnerable in Alzheimer’s disease have very long thin extensions called axons, which the cells use to communicate with other cells within the same region, or to talk to other regions of the brain. These axons also help move essential nutrients, proteins and other molecules to and from the central part of the cell; this important function is performed by proteins collectively known as molecular motors. One of the earliest signs of disease is the shrinkage, distortion, and degeneration of some of these long extensions and the loss of their connections to other brain cells. These findings suggest that the mechanisms of cellular transport may be impaired in the early stages of Alzheimer’s disease. It is possible that the impaired transport in axons (axonal transport) contributes to brain cell vulnerability and brain cell death during the Alzheimer’s disease process.
Scott Brady, Ph.D., and colleagues have been studying axonal transport and molecular motors in brain cells and how they are affected by Alzheimer’s-like diseases in animal models. They have proposed to study how axonal transport is controlled by specific biochemical pathways in the cell, and how it is affected by beta-amyloid and tau, two proteins implicated in the brain changes associated with Alzheimer’s disease. These studies will improve our understanding of why some brain cells are especially vulnerable to damage and death during Alzheimer’s disease, and they may suggest ways to counteract that vulnerability.