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Alzheimer's Disease Research - Current Award

Dr. Kelly Dineley

Kelley Dineley, Ph.D.

University of Texas Medical Branch
Galveston, TX

Title: PPAR-Gamma Rescue Of Cognitive Function In Alzheimer's Disease
Non-Technical Title: Insulin Regulatory Gene In The Central Nervous System Mediates Cognitive Function In Alzheimer's Disease

Co-Investigator(s):
Larry Denner, Ph.D.
University of Texas Medical Branch

Duration: April 1, 2009 - March 31, 2012
Award Type: Standard
Award Amount: $399,000


Summary:

Our preliminary studies have discovered a role for a gene called PPAR-gamma in cognitive function in Alzheimer's disease. Since virtually nothing is known about PPAR-gamma regulation in the brain, the specific aims of this project are to define the PPAR-gamma signaling axis in brain regions that underlie the types of cognitive function that PPAR-gamma agonism improves.

Details:


Recent clinical studies implicate insulin resistance as an important risk factor for Alzheimer's disease. A very successful diabetes treatment is PPAR-gamma agonism to increase insulin sensitivity. Unfortunately, this class of drug has serious side effects to peripheral organs including the heart. We have discovered that stimulating PPAR-gamma in the brain can reverse cognitive deficits in an Alzheimer's animal model that shows insulin resistance like humans with Alzheimer's. This project will lead to an understanding of how brain PPAR-gamma functions in learning and memory in Alzheimer's disease. This will lead to more selective (i.e., lacking peripheral side effects) cognitive-enhancing agents for Alzheimer's disease patients.

Progress Updates:

During the first year of our AHAF award, we have aggressively tackled our proposed studies to understand the role of PPAR-gamma in the rescue of cognitive function in Alzheimer's disease (AD). Normally, the function of PPAR-gamma is to regulate glucose (sugar) and lipid (fat) metabolism and suppress inflammatory gene expression. This year we have developed the necessary tools and reagents to measure the activities of transcription factor PPAR-gamma and related proteins in a mouse model of AD, called Tg2576. Tg2576 is a transgenic model of amyloid pathology, with measurable levels of amyloid protein expression, that develop amyloid plaque deposits in the cortex, hippocampus and amygdala of the brain by 10 months of age. The hippocampus of Tg2576 mice will be tested, following cognitive rescue through treatment with the PPAR-gamma agonist drug, rosiglitazone. These studies for the first time will provide us with an understanding of how PPAR-gamma is regulated in the brain, at the molecular level.