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

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Affiliations

  • 1. Centre for Immunology and University of New South Wales, School of Medicine and School of Medical Sciences, Sydney, Australia.
      Authors
    • Guillemin GJ 1
    (1 author)

ORCIDs linked to this article

Neuro-degenerative Diseases, 01 Jan 2005, 2(3-4):166-176
https://doi.org/10.1159/000089622 PMID: 16909022 

Review

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.

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