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

Zhiyou Cai, M. Delwar Hussain, Liang Jun Yan

Research output: Contribution to journalReview article

130 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)307-321
Number of pages15
JournalInternational Journal of Neuroscience
Volume124
Issue number5
DOIs
StatePublished - May 2014

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Amyloid beta-Peptides
Microglia
Alzheimer Disease
Amyloid Plaques
Chemokines
Amyloid
Free Radicals
Molecular Biology
Anti-Idiotypic Antibodies
Anti-Inflammatory Agents
Clinical Trials
Cytokines
Inflammation
Research
Pharmaceutical Preparations

Keywords

  • Alzheimer's disease
  • Beta-amyloid
  • Microglia
  • Neuroinflammation

Cite this

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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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Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease. / Cai, Zhiyou; Hussain, M. Delwar; Yan, Liang Jun.

In: International Journal of Neuroscience, Vol. 124, No. 5, 05.2014, p. 307-321.

Research output: Contribution to journalReview article

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