On the origin of Alzheimer's disease. Trials and tribulations of the amyloid hypothesis.

Abstract:

:The amyloid cascade hypothesis, which implicates the amyloid Aβ peptide as the pathological initiator of both familial and sporadic, late onset Alzheimer's disease (AD), continues to guide the majority of research. We believe that current evidence does not support the amyloid cascade hypothesis for late onset AD. Instead, we propose that Aβ is a key regulator of brain homeostasis. During AD, while Aβ accumulation may occur in the long term in parallel with disease progression, it does not contribute to primary pathogenesis. This view predicts that amyloid-centric therapies will continue to fail, and that progress in developing successful alternative therapies for AD will be slow until closer attention is paid to understanding the physiological function of Aβ and its precursor protein.

journal_name

Ageing Res Rev

journal_title

Ageing research reviews

authors

Castello MA,Soriano S

doi

10.1016/j.arr.2013.10.001

subject

Has Abstract

pub_date

2014-01-01 00:00:00

pages

10-2

eissn

1568-1637

issn

1872-9649

pii

S1568-1637(13)00068-8

journal_volume

13

pub_type

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