The DOI matches its Crossref record; 233 of the 234 references it cites were found in a registry or an index.
Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease
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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“Aβ, especially the Aβ1-42 oligomer and fibril, is an established instigator of neuroinflammation (Cai et al., 2014).”
From LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease (2019) · cites this paper as Cai et al., 2014
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Metadata
- 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
- 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
- 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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