Understanding this process has direct relevance for therapy of AD and might suggest the possibility that cholinergic agents might regulate the cellular processing of beta-amyloid precursor protein, thereby controlling the process of amyloidogenesis.
Apoptosis influences early development and later refinement in adult tissues.
Specially, I am examining the hypothesis that neuronal apoptosis results from the activation of an endogenous genetic program in an in vitro model of naturally occurring neuronal death. Our model system is based on characterizing the expression of neuronal genes in sympathetic neurons which undergo programmed cell death after deprivation of nerve growth factor. Currently my laboratories are supported by a NIH grant and some monies from the drug company and Indiana Division of Mental Health. Melatonin affects the metabolism of the beta-amyloid precursor protein in different cell types. Functional identification of the promoter of the gene encoding the Rhesus monkey beta-amyloid precursor protein.