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2008 Grants - LaDu
The Effect of ApoE isoform on Intraneuronal ApoE/Abeta42 Interactions
Mary Jo LaDu, Ph.D.
University of Illinois, Chicago
2008 Zenith Fellows Award
Much Alzheimer research has focused on the protein fragment beta-amyloid and the APOE gene. Beta-amyloid tends to accumulate into structures called plaques in the Alzheimer brain. These plaques are thought to disrupt cell-to-cell communication and cause cell death. APOE provides the genetic "blueprint" for the protein apolipoprotein E, which plays a role in transporting lipids (fats) into cells. A variant of APOE called APOE-e4 has been identified as a potential risk factor for Alzheimer's.
Mary Jo LaDu, Ph.D., and colleagues hypothesize that beta-amyloid and APOE interact with each other in specific ways that may lead to Alzheimer's. For example, APOE-e4 has been shown to facilitate the accumulation of beta-amyloid in the brain. For this proposal, Dr. LaDu's group will study the effects of beta-amyloid/APOE interactions in cultured cells and in mice genetically engineered to produce Alzheimer-like symptoms. The researchers will treat the cultured cells with beta-amyloid and with one of three variants of APOE—APOE-e2, APOE-e3 or APOE-e4. They will engineer the mice to overproduce both beta-amyloid and one of the three APOE variants. Dr. LaDu's team will then look to see where precisely beta-amyloid/APOE interactions occur in both the cells and the mice brains. They will also look for correlations between these interactions and cellular damage.
The results of this study should lead to a better understanding of the roles both beta-amyloid and APOE play in Alzheimer's disease. Such knowledge could lead to novel therapies for the disease.