title: A century of Alzheimer's disease.
abstract: One hundred years ago a small group of psychiatrists described the abnormal protein deposits in the brain that define the most common neurodegenerative diseases. Over the past 25 years, it has become clear that the proteins forming the deposits are central to the disease process. Amyloid-beta and tau make up the plaques and tangles of Alzheimer's disease, where these normally soluble proteins assemble into amyloid-like filaments. Tau inclusions are also found in a number of related disorders. Genetic studies have shown that dysfunction of amyloid-beta or tau is sufficient to cause dementia. The ongoing molecular dissection of the neurodegenerative pathways is expected to lead to a true understanding of disease pathogenesis.
authors.affiliation: Laboratory of Molecular Biology, Medical Research Council, Cambridge CB2 2QH, UK. mg@mrc-lmb.cam.ac.uk
authors.forename: Michel
authors.initials: M
authors.lastname: Goedert
authors.forename: Maria Grazia
authors.initials: MG
authors.lastname: Spillantini
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000266:history / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry; D049673:History, 20th Century; D006801:Humans; D009154:Mutation; D016874:Neurofibrillary Tangles / Q000737:chemistry / Q000473:pathology; D058225:Plaque, Amyloid / Q000737:chemistry / Q000473:pathology; D053764:Presenilin-1 / Q000235:genetics / Q000378:metabolism; D016875:tau Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D001057:Apolipoproteins E; D053764:Presenilin-1; D016875:tau Proteins