Synaptic Impairment in Alzheimer's Disease: A Dysregulated Symphony

被引：315

作者：

Forner, Stefania ^{[1
]}

Baglietto-Vargas, David ^{[1
]}

Martini, Alessandra C. ^{[1
]}

Trujillo-Estrada, Laura ^{[1
]}

LaFerla, Frank M. ^{[1
,2
]}

机构：

[1] Univ Calif Irvine, Inst Memory Impairments & Neurol Disorders, Irvine, CA 92697 USA

[2] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA

来源：

TRENDS IN NEUROSCIENCES | 2017年 / 40卷 / 06期

关键词：

AMYLOID-BETA OLIGOMERS; CELLULAR PRION PROTEIN; GLUTAMATE-RECEPTOR; 5; A-BETA; TAU OLIGOMERS; WILD-TYPE; MITOCHONDRIAL DYSFUNCTION; COGNITIVE IMPAIRMENTS; PATHOLOGICAL TAU; MOUSE MODEL;

D O I：

10.1016/j.tins.2017.04.002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodegeneration, not only as a result of the extracellular accumulation of beta-amyloid peptide (Ab) and intracellular accumulation of tau, but also as a consequence of the dysfunction and loss of synapses. Although significant advances have been made in our understanding of the relationship of the pathological role of Ab and tau in synapse dysfunction, several questions remain as to how Ab and tau interdependently cause impairments in synaptic function in AD. Overall, more insight into these questions should enable researchers in this field to develop novel therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating disease.

引用

页码：347 / 357

页数：11

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