Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer’s Disease

Joint Authors

Xie, Jingdun
Wang, Haitao
Lin, Ting
Bi, Bing-Tian

Source

BioMed Research International

Issue

Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-11, 11 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2017-04-03

Country of Publication

Egypt

No. of Pages

11

Main Subjects

Medicine

Abstract EN

The main hallmarks of Alzheimer’s disease (AD) are extracellular deposits of amyloid plaques and intracellular accumulation of hyperphosphorylated neurofibrillary tangles (tau).

However, the mechanisms underlying these neuropathological changes remain largely unclear.

To date, plenty of studies have shown that microglia-mediated neuroinflammation contributes to the pathogenesis of AD, and the microglia-synapse pathways have been repeatedly identified as the crucial factor in the disease process.

In this review, evidences from microglia and synapse studies are presented, and the role of microglia in the pathogenesis of AD, the contributing factors to synapse dysfunction, and the role and mechanisms of microglia-synapse pathways will be discussed.

American Psychological Association (APA)

Xie, Jingdun& Wang, Haitao& Lin, Ting& Bi, Bing-Tian. 2017. Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer’s Disease. BioMed Research International،Vol. 2017, no. 2017, pp.1-11.
https://search.emarefa.net/detail/BIM-1135626

Modern Language Association (MLA)

Xie, Jingdun…[et al.]. Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer’s Disease. BioMed Research International No. 2017 (2017), pp.1-11.
https://search.emarefa.net/detail/BIM-1135626

American Medical Association (AMA)

Xie, Jingdun& Wang, Haitao& Lin, Ting& Bi, Bing-Tian. Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer’s Disease. BioMed Research International. 2017. Vol. 2017, no. 2017, pp.1-11.
https://search.emarefa.net/detail/BIM-1135626

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-1135626