Amyloid-β and Tau at the Crossroads of Alzheimer’s Disease

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

28 Scopus citations

Abstract

Alzheimer’s disease (AD) is the most common form of dementia characterized neuropathologically by senile plaques and neurofibrillary tangles (NFTs). Early breakthroughs in AD research led to the discovery of amyloid-β as the major component of senile plaques and tau protein as the major component of NFTs. Shortly following the identification of the amyloid-β (Aβ) peptide was the discovery that a genetic mutation in the amyloid precursor protein (APP), a type1 transmembrane protein, can be a cause of autosomal dominant familial AD (fAD). These discoveries, coupled with other breakthroughs in cell biology and human genetics, have led to a theory known as the “amyloid hypothesis”, which postulates that amyloid-β is the predominant driving factor in AD development. Nonetheless, more recent advances in imaging analysis, biomarkers and mouse models are now redefining this original hypothesis, as it is likely amyloid-β, tau and other pathophysiological mechanism such as inflammation, come together at a crossroads that ultimately leads to the development of AD.

Original languageEnglish
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer
Pages187-203
Number of pages17
DOIs
StatePublished - 2019

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1184
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

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