title: Amyloid β: Walking on the dark side of the moon.
abstract: For some decades, amyloid β (Aβ) has only been considered as a cytotoxic peptide, putative cause and marker of Alzheimer's disease (AD). Today, however, a considerable amount of evidence goes against the classical amyloid hypothesis and illustrates a new picture in which the Aβ loss of function, rather than its accumulation, has a pathogenic role in AD. In this concise review, we summarize some highlights of a collection of research pointing to the physiological function of Aβ and its role in the mechanisms of memory formation.
authors.affiliation: Department of Pharmacy and Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy.
authors.forename: Ernesto
authors.initials: E
authors.lastname: Fedele
authors.affiliation: Department of Experimental Medicine, University of Genoa, Genoa, Italy.
authors.forename: Daniela
authors.initials: D
authors.lastname: Rivera
authors.affiliation: Department of Experimental Medicine, University of Genoa, Genoa, Italy.
authors.forename: Barbara
authors.initials: B
authors.lastname: Marengo
authors.affiliation: Department of Experimental Medicine, University of Genoa, Genoa, Italy.
authors.forename: Maria A
authors.initials: MA
authors.lastname: Pronzato
authors.affiliation: Department of Experimental Medicine, University of Genoa, Genoa, Italy. Electronic address: ricciarelli@medicina.unige.it.
authors.forename: Roberta
authors.initials: R
authors.lastname: Ricciarelli
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D006801:Humans; D008568:Memory
chemical_list: D016229:Amyloid beta-Peptides
keywords: Alzheimer’s disease; Amyloid β; Long term potentiation; Memory; cAMP