Amyloid β: Walking on the dark side of the moon

被引：18

作者：

Fedele, Ernesto ^{[1
,2
]}

Rivera, Daniela ^{[3
]}

Marengo, Barbara ^{[3
]}

Pronzato, Maria A. ^{[3
]}

Ricciarelli, Roberta ^{[3
]}

机构：

[1] Univ Genoa, Dept Pharm, Genoa, Italy

[2] Univ Genoa, Ctr Excellence Biomed Res, Genoa, Italy

[3] Univ Genoa, Dept Expt Med, Genoa, Italy

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2015年 / 152卷

关键词：

Alzheimer's disease; Amyloid beta; cAMP; Long term potentiation; Memory; NICOTINIC ACETYLCHOLINE-RECEPTORS; HIPPOCAMPAL SYNAPTIC PLASTICITY; ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; ALPHA-SECRETASE; MICE LACKING; WILD-TYPE; MEMORY; PEPTIDE; DEFICITS;

D O I：

10.1016/j.mad.2015.09.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

For some decades, amyloid beta (A beta) has only been considered as a cytotoxic peptide, putative cause and marker of Alzheimer's disease (AD). Today, however, a considerable amount of evidence goes against the classical amyloid hypothesis and illustrates a new picture in which the A beta loss of function, rather than its accumulation, has a pathogenic role in AD. In this concise review, we summarize some highlights of a collection of research pointing to the physiological function of A beta and its role in the mechanisms of memory formation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

引用

页码：1 / 4

页数：4

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