The amyloid and beyond; A molecular answer to forget me not.
Alzheimer disease (AD) is associated with aging and is described as a degenerative disorder of the human central nervous system that destroys the brain and leaves its victims unable to function on their own. Mutations in the presenilin-1 (PS1)gene are associated with the most aggressive subtype of Familial Alzheimer Disease (between 25 and 60 years of age). Although PS1 is a key element in the AD puzzle, the cellular role and regulation of both normal and mutant forms remains to be unambiguously identified. Presenilin is required for amyloid formation, cell differentiation and developmental signaling. The overall goal of my research project is to identify the biological function of PS1 and to elucidate the biochemical pathways in which the mutated form of this protein leads to the neurodegeneration observed in AD. Results derived from this proposal will help elucidate PS1 biological functions both in amyloid formation and cell signaling. We also propose to develop a new therapeutic tool to decrease the accumulation of amyloid in the brain of Alzheimer disease patient. Altogether, our results will assist in the development of novel treatments for Alzheimer disease. Therefore, this project has a significant chance of improving the quality of life of aging people.