The role of beta amyloid in Alzheimer's disease: still a cause of everything or the only one who got caught?

G. Verdile, S. Fuller, C.S. Atwood, S.M. Laws, S.E. Gandy, Ralph Martins

Research output: Contribution to journalReview article

123 Citations (Scopus)

Abstract

The beta amyloid (Abeta) protein is a key molecule in the pathogenesis of Alzheimer's disease (AD). The tendency of the Abeta peptide to aggregate, its reported neurotoxicity, and genetic linkage studies, have led to a hypothesis of AD pathogenesis that many AD researchers term the amyloid cascade hypothesis. In this hypothesis, an increased production of Abeta results in neurodegeneration and ultimately dementia through a cascade of events. In the past 15 years, debate amongst AD researchers has arisen as to whether Abeta is a cause or an effect of the pathogenic process. Recent in vitro and in vivo research has consolidated the theory that Abeta is the primary cause, initiating secondary events, culminating in the neuropathological hallmarks associated with AD. This research has led to the development of therapeutic agents, currently in human clinical trials, which target Abeta. (C) 2004 Elsevier Ltd. All rights reserved.
Original languageEnglish
Pages (from-to)397-409
JournalPharmacological Research
Volume50
DOIs
Publication statusPublished - 2004

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