The Effect of Beclin 1 on Neurodegeneration in Alzheimer's Disease and Aging
Alzheimer’s Disease (AD) affects a growing number of the elderly and results in a progressive loss of memory. The brains of people with AD usually show a characteristic accumulation of abnormal proteins called beta amyloid (Aβ) and tau. Associated with abnormal protein build-up is the appearance of unhealthy brain cells and brain cell death. The cause of AD is currently unclear, but age is known to be the greatest risk factor. Therefore it is believed that cellular processes that maintain brain cell health and clearance of protein aggregates are dysfunctional with age and during disease.
My research is interested in studying whether a protein degradation process, called autophagy (meaning to “eat oneself”), may influence both brain cell health and abnormal protein accumulation during AD. Autophagy normally helps cells survive when they do not have sufficient nutrients. Autophagy also plays a role in clearing abnormal proteins. Interestingly, recent evidence from our lab suggests that Beclin 1 (a protein essential for autophagy) is reduced in AD brains. Thus my Hillblom Foundation Fellowship aims to investigate the consequence of reduced Beclin 1 expression on brain cell health and whether overexpressing Beclin 1 may protect against brain cell death and improve clearance of Aβ during AD. Our studies may not only help in gaining a better understanding of why brain cells are unhealthy in AD, but also identify potential new targets for the treatment of diseases that cause brain cell death.