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Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease
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...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394358/ https://www.ncbi.nlm.nih.gov/pubmed/28473983 http://dx.doi.org/10.1155/2017/2986460 |
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author | Xie, Jingdun Wang, Haitao Lin, Ting Bi, Bingtian |
author_facet | Xie, Jingdun Wang, Haitao Lin, Ting Bi, Bingtian |
author_sort | Xie, Jingdun |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5394358 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-53943582017-05-04 Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease Xie, Jingdun Wang, Haitao Lin, Ting Bi, Bingtian Biomed Res Int Review Article 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. Hindawi 2017 2017-04-03 /pmc/articles/PMC5394358/ /pubmed/28473983 http://dx.doi.org/10.1155/2017/2986460 Text en Copyright © 2017 Jingdun Xie et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Xie, Jingdun Wang, Haitao Lin, Ting Bi, Bingtian Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title | Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title_full | Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title_fullStr | Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title_full_unstemmed | Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title_short | Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer's Disease |
title_sort | microglia-synapse pathways: promising therapeutic strategy for alzheimer's disease |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394358/ https://www.ncbi.nlm.nih.gov/pubmed/28473983 http://dx.doi.org/10.1155/2017/2986460 |
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