Journal
NEUROTOXICITY RESEARCH
Volume 7, Issue 1-2, Pages 103-123Publisher
SPRINGER
DOI: 10.1007/BF03033781
Keywords
quinolinic acid; kynurenine; kynurenic acid; HIV; AIDS; dementia; inflammatory brain disease; cytokines; chemokines; N-methyl-D-aspartate; macrophages; microglia
Categories
Ask authors/readers for more resources
Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous brain excitotoxin when produced and released by activated macrophages/microglia, the very cells that are prominent in the pathogenesis of ADC. This review examines QUIN's involvement in the features of ADC and its role in pathogenesis. We then synthesize these findings into a hypothetical model for the role played by QUIN in ADC, and discuss the implications of this model for ADC and other inflammatory brain diseases.
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