Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease.
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| Title: | Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease. |
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| Authors: | Cai, Zhiyou (AUTHOR), Hussain, M. Delwar (AUTHOR), Yan, Liang-Jun (AUTHOR) |
| Source: | International Journal of Neuroscience. May2014, Vol. 124 Issue 5, p307-321. 15p. |
| Subjects: | Microglia, Basal ganglia diseases, Alzheimer's disease, Glycoproteins, Apolipoprotein E4 |
| Abstract: | Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis by releasing inflammatory mediators such as inflammatory cytokines, complement components, chemokines, and free radicals that are all known to contribute to beta-amyloid (A β) production and accumulation. On the other hand, microglia are also known to play a beneficial role in generating anti-A β antibodies and stimulating clearance of amyloid plaques. A β itself, an inducer of microglia activation and neuroinflammation, has been considered as an underlying and unifying factor in the development of AD. A vicious cycle of inflammation has been formed between A β accumulation, activated microglia, and microglial inflammatory mediators, which enhance A β deposition and neuroinflammation. Thus, inhibiting the vicious cycle seems to be a promising treatment to restrain further development of AD. With increasing research efforts on microglia in AD, intervention of microglia activation and neuroinflammation in AD may provide a potential target for AD therapy in spite of the provisional failure of nonsteroidal antiinflammatory drugs in clinical trials. [ABSTRACT FROM AUTHOR] |
| Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis by releasing inflammatory mediators such as inflammatory cytokines, complement components, chemokines, and free radicals that are all known to contribute to beta-amyloid (A β) production and accumulation. On the other hand, microglia are also known to play a beneficial role in generating anti-A β antibodies and stimulating clearance of amyloid plaques. A β itself, an inducer of microglia activation and neuroinflammation, has been considered as an underlying and unifying factor in the development of AD. A vicious cycle of inflammation has been formed between A β accumulation, activated microglia, and microglial inflammatory mediators, which enhance A β deposition and neuroinflammation. Thus, inhibiting the vicious cycle seems to be a promising treatment to restrain further development of AD. With increasing research efforts on microglia in AD, intervention of microglia activation and neuroinflammation in AD may provide a potential target for AD therapy in spite of the provisional failure of nonsteroidal antiinflammatory drugs in clinical trials. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00207454 |
| DOI: | 10.3109/00207454.2013.833510 |
