AMYLOID BETA-PEPTIDE AND OXIDATIVE CELLULAR INJURY IN ALZHEIMERS-DISEASE

Alzheimer's disease is a progressive neurodegenerative disorder that a ffects primarily learning and memory functions. There is significant n euronal loss and impairment of metabolic functioning in the temporal l obe, an area believed to be crucial for learning and memory tasks. Agg regated deposits of amyloid beta-peptide may have a causative role in the development and progression of AD. We review the cellular actions of A beta and how they can contribute to the cytotoxicity observed in AD. A beta causes plasma membrane lipid peroxidation, impairment of io n-motive ATPases, glutamate uptake, uncoupling of a G-protein Linked r eceptor, and generation of reactive oxygen species. These effects cont ribute to the loss of intracellular calcium homeostasis reported in cu ltured neurons. Many cell types other than neurons show alterations in the Alzheimer's brain. The effects of A beta on these cell types is a lso reviewed.