Abstract

Alzheimer’s disease (AD) is pathologically characterized by accumulation of cortical neuritic plaques. Neuritic plaques are composed of a central core of amyloid-beta (AB). Peptide is associated with reactive microglia. Evidence suggests that deposition of AB is a primary step in a cascade of events that leads to AD. Three genetic mutations that cause early onset, autosomal dominant familial AD in the amyloid precursor protein, PS1 and PS2 (chromosomes 21, 14 and 1) result in the increased production of AB. Therapeutic interventions that prevent deposition of AB or promote its clearance could be a viable strategy for disease treatment and/or prevention. Immunotherapy for AD has attracted a great deal of attention: active (vaccination) and passive immunotherapy in animal models. Vaccination is benign and effective in phase I and II trials in humans. Around 200 patients in phase I tolerated the vaccine, however, about 6% of 300 patients in a phase II study developed acute autoimmune meningoecephalitis and the trial was stopped. Substantial slowing of cognitive decline was recorded in vaccinated patients.

When treating patients with Alzheimer’s disease or vascular dementia, the uncompetitive, moderate-affinity, voltage-dependent NMDA antagonist with fast receptor kinetics Memantine has proved effective on three independent levels: cognition, function, and clinical global change. This pathogenetic treatment also has a neuroprotective potential and has a superior safety profile.