Cited by 382Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsPhagocytosis and Immune Regulation

Microglia and inflammatory mechanisms in the clearance of amyloid β peptide

Open access
Rogers, Joseph, Strohmeyer, Ron, Kovelowski, C.J., Li, Rena·2002·Glia

Abstract

There is now abundant evidence that brain microglia, when activated, have the lineage, receptors, and synthetic capacity to participate in both potentially neurotoxic inflammatory responses and potentially beneficial phagocytic responses. Amyloid beta peptide (Abeta) forms highly insoluble, beta-pleated aggregates that are widely deposited in the Alzheimer's disease (AD) cortex and limbic system. Aggregated Abeta also activates the classical and alternative complement cascades. These properties make Abeta an excellent target for microglial phagocytosis, a view supported by multiple reports, through well established mechanisms of phagocyte clearance.

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Crossref · 10.1002/glia.10153

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  • In AD, microglia and astrocytes can promote clearance of Aβ; if they are not able to do that, accumulation of Aβ deposits leads to neuronal death.

    “In AD, these cells can promote the clearance of Aβ, however, if they are not able to do that, there is an accumulation of Aβ deposits leading to neuronal death (Rogers et al., 2002).”

    From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Rogers et al., 2002

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5 of the 142 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Abbas AK, Lichtman AH, Pober JS. 1994a. Antibodies and antigens. In: Abbas AK, Lichtman AH, Pober JS, editors. Cellular and mo- lecular immunology. Philadelphia: WB Saunders. p 33-64.
  2. Rogers J, Lue L-F, Walker DG, Yan SD, Stern D, Strohmeyer R, Kovelowski CJ. 2002. Elucidating molecular mechanisms of Alzhei- mer's disease in culture models, in neuroinflammation-from bench to bedside. Heidelberg: Springer. p 25-44.

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Authors
Rogers, J., Strohmeyer, R., Kovelowski, C. J., & Li, R.
Affiliations
Banner Sun Health Research Institute (US)
Corresponding author
Rogers, Joseph
Venue
Glia
Publisher
Wiley
Published
2002-10-04
Volume
40
Issue
2
Pages
260-269
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
OpenAlex
W2046704592
Cited by
381
References
142
Citations by year
2026: 6 · 2025: 10 · 2024: 9 · 2023: 6 · 2022: 10 · 2021: 15 · 2020: 9 · 2019: 11 · 2018: 12 · 2017: 8 · 2016: 12 · 2015: 14 · 2014: 19 · 2013: 17 · 2012: 18
FWCI
1.98
Type
journal article
Language
en
Open access
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Alzheimer's Association
  • National Institute on Aging (AGO7367)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords
microglia, amyloid-beta, Alzheimer's disease, microglial phagocytosis, neuroinflammation, complement system, microglial activation
MeSH terms
Alzheimer Disease, Animals, Antigen-Antibody Complex, Antigens, Chemotaxis, Encephalitis, Humans, Phagocytosis, Amyloid beta-Peptides, Microglia

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