Cited by 587Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

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Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease

Cai, Zhiyou, Hussain, M. Delwar, Yan, Liang-Jun·2014·International Journal of Neuroscience

DOI 10.3109/00207454.2013.833510

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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 (Aβ) production and accumulation. On the other hand, microglia are also known to play a beneficial role in generating anti-Aβ antibodies and stimulating clearance of amyloid plaques. Aβ 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 Aβ accumulation, activated microglia, and microglial inflammatory mediators, which enhance Aβ 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.

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Additional file 6 of Inhibition of NLRP1 inflammasome improves autophagy dysfunction and Aβ disposition in APP/PS1 mice
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Additional file 3 of The involvement of NLRP3 inflammasome in CUMS-induced AD-like pathological changes and related cognitive decline in mice
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Additional file 3 of Inhibition of NLRP1 inflammasome improves autophagy dysfunction and Aβ disposition in APP/PS1 mice
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Additional file 4 of Inhibition of NLRP1 inflammasome improves autophagy dysfunction and Aβ disposition in APP/PS1 mice
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Additional file 2 of The involvement of NLRP3 inflammasome in CUMS-induced AD-like pathological changes and related cognitive decline in mice
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Additional file 5 of Inhibition of NLRP1 inflammasome improves autophagy dysfunction and Aβ disposition in APP/PS1 mice
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Authors: Cai, Z., Hussain, M. D., & Yan, L.-J.
Affiliations: Anhui Medical University (CN)
Texas A&M Health Science Center (US)
University of North Texas Health Science Center (US)
Corresponding author: Cai, Zhiyou
ORCID: Cai, Zhiyou
Hussain, M. Delwar
Yan, Liang-Jun
Venue: International Journal of Neuroscience
Publisher: Informa UK Limited
Published: 2013-09-12
Volume: 124
Issue: 5
Pages: 307-321
ISSN: 0020-7454 (ISSN-L)
1543-5245
DOI: 10.3109/00207454.2013.833510
OpenAlex: W2096407545
Cited by: 583
References: 234
Citations by year: 2026: 17 · 2025: 45 · 2024: 72 · 2023: 86 · 2022: 67 · 2021: 82 · 2020: 72 · 2019: 54 · 2018: 45 · 2017: 13 · 2016: 14 · 2015: 12 · 2014: 3 · 2013: 1
FWCI: 0.97
Type: journal article
Language: en
Open access: closed
Locations: International Journal of Neuroscience (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: microglia, neuroinflammation, amyloid-beta, Alzheimer's disease, microglial activation, inflammatory cytokines, complement system, chemokines, free radicals, amyloid plaque clearance, anti-amyloid antibodies, anti-inflammatory therapy
MeSH terms: Alzheimer Disease, Humans, Inflammation, Amyloid beta-Peptides, Microglia

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Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease

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