Defining the Roles of Presenilin-1 and Presenilin-2 in Aβ Metabolism

Abstract

Therapeutics targeting beta amyloid build up in the brain have shown some clinical benefits in Alzheimer’s disease. Further insights into such drug targets is required to improve clinical outcomes. This thesis provided novel, mechanistic insights into how proteins called Presenilins generate and remove beta amyloid. The findings provide the foundation to pursue the Presenilins as drug targets for Alzheimer’s disease to reduce the production and improve removal of beta amyloid from the brain.