title: Ionic effects of the Alzheimer's disease beta-amyloid precursor protein and its metabolic fragments.
abstract: 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.
authors.affiliation: Dept of Biology, Imperial College of Science, Technology and Medicine, London, UK.
authors.forename: S P
authors.initials: SP
authors.lastname: Fraser
authors.forename: Y H
authors.initials: YH
authors.lastname: Suh
authors.forename: M B
authors.initials: MB
authors.lastname: Djamgoz
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism
chemical_list: D016564:Amyloid beta-Protein Precursor; D007473:Ion Channels