Milar to that of AD. b-amyloid is a potent and direct neurotoxic agent [77-79], much like the HIV-1 proteins gp120 and Tat, and it induces a cascade of cellular mechanisms including activation of microglia [80], which leads to neuronal damage [81]. Indeed, reactive microglia are closely associated with neuritic and b-amyloid plaques, just as they are with HIV1 Tat protein [82-89]. Using electron m