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Research Grants 2011

To view an abstract, select an author from the vertical list on the left.

2011 Grants - Pigino

Mechanism Underlying Oligomeric Abeta-Induced Axonal Transport Dysfunction

Gustavo F. Pigino, Ph.D.
University of Illinois at Chicago
Chicago, Illinois

2011 New Investigator Research Grant to Promote Diversity

Beta-amyloid (also known as Abeta) is a protein fragment known to be toxic to nerve cells and implicated in Alzheimer's disease. However, the mechanisms by which beta-amyloid leads to nerve cell toxicity are not well understood.

Beta-amyloid is known to aggregate into large structures known as amyloid plaques, and into smaller structures containing a few copies of beta-amyloid, known as oligomers. In recent years, scientists have found increasing evidence that beta-amyloid oligomers are the most toxic form, and may be the leading cause of neurodegeneration.

Gustavo F. Pigino, Ph.D. and colleagues are studying how beta-amyloid oligomers are toxic to nerve cells. They have found evidence that beta-amyloid oligomers inhibit the ability of nerve cells to transport nutrients to distant regions of the cell, thereby damaging the ability of the cells to function and send signals to other nerve cells.

The researchers have proposed to use nerve cells growing in controlled conditions, as well as mice that have been genetically altered to express Alzheimer-like pathology, to study how beta-amyloid oligomers inhibit nutrient transport in nerve cells. They plan to focus on the receptors and signaling pathways that are critical for nutrient transport, and examine how they are affected by treatment of the cells with beta-amyloid oligomers. These studies may shed light on some of the earliest steps in the development of Alzheimer's pathology, and may identify targets for future treatments to prevent or slow disease progression.

Alzheimer's Association International Conference | July 16-20, 2017, London, England

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