The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer's Disease

被引：21

作者：

Ziegler-Waldkirch, Stephanie ^{[1
,2
]}

Meyer-Luehmann, Melanie ^{[1
,2
]}

机构：

[1] Univ Freiburg, Dept Neurol, Med Ctr, Freiburg, Germany

[2] Univ Freiburg, Fac Med, Freiburg, Germany

来源：

FRONTIERS IN CELLULAR NEUROSCIENCE | 2018年 / 12卷

关键词：

Alzheimer's disease; amyloid plaques; glial cells; synapse loss; microglia; astrocytes; AMYLOID-BETA-PROTEIN; LONG-TERM POTENTIATION; GENOME-WIDE ASSOCIATION; ENVIRONMENTAL ENRICHMENT; IN-VIVO; TRANSGENIC MICE; COMPLEMENT ACTIVATION; REACTIVE ASTROCYTES; IDENTIFIES VARIANTS; SOLUBLE OLIGOMERS;

D O I：

10.3389/fncel.2018.00473

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer's disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropathological hallmarks are amyloid-beta (A beta) plaques and neurofibrillary tangles. In the brain of AD patients and in mouse models of AD several morphological and functional changes, such as microgliosis and astrogliosis around A beta plaques, as well as dendritic and synaptic alterations, are associated with these lesions. In this review article, we will summarize the current literature on synapse loss in mouse models of AD and discuss current and prospective treatments for AD.

引用

页数：8

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