A beta 1-42 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 journalArticle

90 Citations (Scopus)

Abstract

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 A beta 1-42 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, A beta 1-40 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
JournalNeuroReport
Volume14
Issue number18
Publication statusPublished - 19 Dec 2003
Externally publishedYes

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