Aβ1-42 induces production of quinolinic acid by human macrophages and microglia

Gilles J. Guillemin*, George A. Smythe, Laura A. Veas, Osamu Takikawa, Bruce J. Brew

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


We hypothesized that the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QUIN), may play an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we demonstrated that aggregated amyloid peptide Aβ1-42 induced indoleamine 2,3-dioxygenase (IDO) expression and resulted in a significant increase in production of QUIN by human primary macrophages and microglia. In contrast, Aβ1-40 and prion peptide (PrP) 106-126 did not induce any significant increase in QUIN production. These data imply that local QUIN production may be one of the factors involved in the pathogenesis of neuronal damage in AD.
Original languageEnglish
Pages (from-to)2311-2315
Number of pages5
Issue number18
Publication statusPublished - 2003
Externally publishedYes


  • 3-dioxygenase
  • Aβ1-42
  • Alzheimer's disease
  • human
  • indoleamine 2
  • macrophages
  • microglia
  • quinolinic acid


Dive into the research topics of 'Aβ1-42 induces production of quinolinic acid by human macrophages and microglia'. Together they form a unique fingerprint.

Cite this