Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease

Joseph Quinn, Thomas Montine, Jason Morrow, William R. Woodward, Doris Kulhanek, Felix Eckenstein

Research output: Contribution to journalArticle

92 Scopus citations

Abstract

The hypothesis that inflammation and beta amyloid deposition are causally linked in Alzheimer's disease (AD) was tested in a transgenic mouse model. Untreated beta amyloid plaque-bearing Tg2576 mice did not differ from wild type animals in brain levels of most inflammatory mediators. Indomethacin treatment suppressed brain levels of prostaglandins by 90%, but reduced hippocampal beta amyloid by only 20%, with no effect on cortical beta amyloid. The discordant effects on beta amyloid and cyclooxygenase (COX) suggest that these effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are not causally linked. Further evidence against a causal relationship is seen in an unexpected trend to lower levels of beta amyloid after an inflammatory stimulus [lipopolysaccharide (LPS)].

Original languageEnglish (US)
Pages (from-to)32-41
Number of pages10
JournalJournal of Neuroimmunology
Volume137
Issue number1-2
DOIs
StatePublished - Apr 2003

Keywords

  • Alzheimer
  • Animal model
  • Cyclooxygenase
  • F2-isoprostanes
  • Indomethacin
  • Nonsteroidal anti-inflammatory drug
  • Oxidative stress

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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