title: Prions, prionoids and pathogenic proteins in Alzheimer disease.
abstract: Like patients with prion disease, Alzheimer patients suffer from a fatal, progressive form of dementia. There is growing evidence that amyloid-β (Aβ) aggregates may be transmissible similar to prions, at least under extreme experimental conditions. However, unlike mice infected with prion protein (PrP) prions, those inoculated with Aβ do not die. The transmission of Aβ and PrP thus differs conspicuously in the neurological effects they induce in their hosts, the difference being no less than a matter of life and death. Far from being a mere academic nuance, this distinction between Aβ and PrP begs the crucial questions of what, exactly, controls prion toxicity and how prion toxicity relates to prion infectivity.
authors.affiliation: Department of Neurology, N. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, MN, USA. hsiao005@umn.edu
authors.forename: Karen H
authors.initials: KH
authors.lastname: Ashe
authors.forename: Adriano
authors.initials: A
authors.lastname: Aguzzi
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000032:analysis / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D006801:Humans; D011328:Prions / Q000032:analysis / Q000378:metabolism* / Q000633:toxicity
chemical_list: D016229:Amyloid beta-Peptides; D011328:Prions