The dark sides of amyloid in Alzheimer's disease pathogenesis

被引：54

作者：

Sorrentino, Pierpaolo ^{[1
]}

Iuliano, Antonietta ^{[2
,3
]}

Polverino, Arianna ^{[2
,3
]}

Jacini, Francesca ^{[2
,3
]}

Sorrentino, Giuseppe ^{[2
,3
]}

机构：

[1] Univ Naples Federico II, Dipartimento Neurosci & Sci Riprod & Odontostomat, Naples, Italy

[2] Univ Naples Parthenope, Dipartimento Sci Motorie & Benessere, I-80133 Naples, Italy

[3] Ist Diag & Cura Hermitage Capodimonte, Naples, Italy

来源：

FEBS LETTERS | 2014年 / 588卷 / 05期

关键词：

Alzheimer's disease; Amyloid; Presenilin; Synaptic plasticity; Neuronal survival; Endo-lysosomal trafficking; Cell cycle regulation; APP INTRACELLULAR DOMAIN; RECEPTOR-RELATED PROTEIN; HUMAN APOLIPOPROTEIN E4; NEURAL STEM-CELLS; PRECURSOR-PROTEIN; TRANSGENIC MICE; BETA-PROTEIN; NEURITE OUTGROWTH; CORTICAL-NEURONS; MOUSE MODEL;

D O I：

10.1016/j.febslet.2013.12.038

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Although widely explored, the pathogenesis of Alzheimer's disease (AD) has yet to be cleared. Over the past twenty years the so call amyloid cascade hypothesis represented the main research paradigm in AD pathogenesis. In spite of its large consensus, the proposed role of beta-amyloid (A beta) remain to be elucidated. Many evidences are starting to cast doubt on A beta as the primary causative factor in AD. For instance, A beta is deposited in the brain following many different kinds of injury. Also, concentration of A beta needed to induce toxicity in vitro are never reached in vivo. In this review we propose an amyloid-independent interpretation of several AD pathogenic features, such as synaptic plasticity, endo-lysosomal trafficking, cell cycle regulation and neuronal survival. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：641 / 652

页数：12

共 169 条

[21] Cytoskeletal Protection: Acting on Notch to Prevent Neuronal Dysfunction [J].