Title

The Role of beta Amyloid in Alzheimer's Disease: Still a Cause of Everything or the Only One Who Got Caught?

Document Type

Journal Article

Publisher

Elsevier

Faculty

Computing, Health and Science

School

Exercise, Biomedical and Health Science

RAS ID

3264

Comments

This article was originally published as: Verdile, G. , Fuller, S., Atwood, C. , Laws, S. , Gandy, S., & Martins, R. N. (2004). The role of beta amyloid in Alzheimer's disease: Still a cause of everything or the only one who got caught?. Pharmacological research, 50(4), 397-409. Original article available here

Abstract

The beta amyloid (Aβ) protein is a key molecule in the pathogenesis of Alzheimer’s disease (AD). The tendency of the Aβ 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 Aβ 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 Aβ is a cause or an effect of the pathogenic process. Recent in vitro and in vivo research has consolidated the theory that Aβ 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 Aβ.

DOI

10.1016/j.phrs.2003.12.028

 

Link to publisher version (DOI)

10.1016/j.phrs.2003.12.028