Implications for the kynurenine pathway and quinolinic acid in amyotrophic lateral sclerosis

Gilles J. Guillemin*, Vincent Meininger, Bruce J. Brew

*Corresponding author for this work

Research output: Contribution to journalReview article

73 Citations (Scopus)

Abstract

The kynurenine pathway (KP) is a major route of L-tryptophan catabolism leading to production of several neurobiologically active molecules. Among them is the excitotoxin quinolinic acid (QUIN) that is known to be involved in the pathogenesis of several major inflammatory neurological diseases. In amyotrophic lateral sclerosis (ALS) degeneration of motor neurons is associated with a chronic and local inflammation (presence of activated microglia and astrocytes). There is emerging evidence that the KP is important in ALS. Recently, we demonstrated that QUIN is significantly increased in serum and CSF of ALS patients. Moreover, most of the factors associated with QUIN toxicity are found in ALS, implying that QUIN may play a substantial role in the neuropathogenesis of ALS. This review details the potential role the KP has in ALS and advances a testable hypothetical model.

Original languageEnglish
Pages (from-to)166-176
Number of pages11
JournalNeurodegenerative Diseases
Volume2
Issue number3-4
DOIs
Publication statusPublished - Jan 2006
Externally publishedYes

Keywords

  • ALS, toxicity pathways
  • Kynurenine pathway
  • Quinolinic acid

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