Alzheimer's disease is a progressive dementia characterized in part by deposition of proteinaceous plaques in various areas of the brain. The main plaque protein component is beta-amyloid, a metabolic product of the beta-amyloid precursor protein. Substantial evidence has implicated beta-amyloid (and other amyloidogenic fragments of the precursor protein) with the neurodegeneration observed in Alzheimer's disease. Recently, beta-amyloid precursor protein and its amyloidogenic metabolic fragments have been shown to alter cellular ionic activity, either through interaction with existing channels or by de novo channel formation. Such alteration in ionic homeostasis has also been linked with cellular toxicity and might provide a molecular mechanism underlying the neurodegeneration seen in Alzheimer's disease.