Microglial responses to amyloid β peptide opsonization and indomethacin treatment

Ronald Strohmeyer, Carl J. Kovelowski, Diego Mastroeni, Brian Leonard, Andrew Grover, Joseph Rogers

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Background: Recent studies have suggested that passive or active immunization with anti-amyloid β peptide, (Aβ) antibodies may enhance microglial clearance of Aβ deposits from the brain, However, in a human clinical trial, several patients developed secondary inflammatory responses in brain that were sufficient to halt the study. Methods: We have used an in vitro culture system to model the responses of microglia, derived from rapid autopsies of Alzheimer's disease patients, to Aβ deposits. Results: Opsonization of the deposits with and-Aβ IgG 6E10 enhanced microglial chemotaxis to and phagocytosis of Aβ, as well as exacerbated microglial secretion of the pro-Inflammatory cytokines TNF-α and IL-6. Indomethacin, a common nonsteroidal anti-inflammatory drug (NSAID), had no effect on microglial chemotaxis or phagocytosis, but did significantly Inhibit the enhanced production of IL-6 after Aβ opsonization. Conclusion: These results are consistent with well known, differential NSAID actions on immune cell functions, and suggest that concurrent NSAID administration might serve as a useful adjunct to Aβ immunization, permitting unfettered clearance of Aβ while dampening secondary, Inflammation-related adverse events.

Original languageEnglish (US)
Article number18
JournalJournal of Neuroinflammation
StatePublished - Aug 19 2005
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology
  • Neurology
  • Cellular and Molecular Neuroscience


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