PhD 1991, (Toxicology) Harvard University
New Research Building, Room WP-13
We study the molecular mechanisms of Alzheimer's disease using a variety of approaches, including animal models, biochemistry, immunohistochemistry, and cell biology. We focus on the strongest genetic risk factor for Alzheimer’s disease: APOE. This gene encodes a protein involved in cholesterol transport and cellular repair. There are three common alleles of APOE: APOE2, APOE3, and APOE4. APOE3 is the most common form; APOE2 (present in about 10% of the US population) lowers the risk of Alzheimer’s disease by 50%; and APOE4 (present in about 25% of the US population) increases the risk by 300%. We are exploring the roles of APOE in the normal regulation of cholesterol metabolism and inflammation in the central nervous system. For this work, we are examining neurons and glia in culture, to look at normal regulation and metabolism of APOE. We are examining the structure of the APOE protein, and its post-translational modifications and association with brain lipoproteins. We are examining mouse models in which the mouse APOE was replaced by the human forms of APOE, studying their sensitivity to brain insults, including exposure to chemotherapeutic agents. Our recent data show that APOE genotype also affects the occurrence of cognitive impairment after chemotherapy, a debilitating side effect of many cancer treatments. Our goals are to understand why APOE affects the risk of Alzheimer’s disease and chemotherapy-induced cognitive impairment so strongly and to define what can be done to lower one’s risk.
The President's Awards for Distinguished Scholar-Teachers at Georgetown University recognize and celebrate the integration of outstanding research and excellence in teaching at our University. The Awards not only honor the individual recipients but also emphasize standards of excellence at Georgetown.
Bill Rebeck, PhD received this honor in 2017.
"The imaging studies could be used in two ways, the researchers say. One is to understand why anatomical and behavioral changes increase Alzheimer’s risk. The other is to help scientists see if experimental neuroprotectant agents are having an effect.
'We are not there, of course. But we are on the cusp of understanding the evolution of a brain that morphs into Alzheimer’s,' Rebeck says."