Journal
NEUROREPORT
Volume 14, Issue 18, Pages 2311-2315Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200312190-00005
Keywords
A beta I-42; Alzheimer's disease; human; indoleamine 2; 3-dioxygenase; macrophages; microglia; quinolinic acid
Categories
Ask authors/readers for more resources
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 Abeta1-42 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, Abeta1-40 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. (C) 2003 Lippincott Williams Wilkins.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available