Kynurenine pathway metabolites as biomarkers for Amyotrophic Lateral Sclerosis

Vanessa X. Tan, Gilles J. Guillemin*

*Corresponding author for this work

Research output: Contribution to journalReview article

4 Citations (Scopus)
7 Downloads (Pure)

Abstract

Amyotrophic Lateral Sclerosis (ALS) currently lacks a robust and well-defined biomarker that can 1) assess the progression of the disease, 2) predict and/or delineate the various clinical subtypes, and 3) evaluate or predict a patient’s response to treatments. The kynurenine Pathway (KP) of tryptophan degradation represent a promising candidate as it is involved with several neuropathological features present in ALS including neuroinflammation, excitotoxicity, oxidative stress, immune system activation and dysregulation of energy metabolism. Some of the KP metabolites (KPMs) can cross the blood brain barrier, and many studies have shown their levels are dysregulated in major neurodegenerative diseases including ALS. The KPMs can be easily analyzed in body fluids and tissue and as they are small molecules, and are stable. KPMs have a Janus face action, they can be either or both neurotoxic and/or neuroprotective depending of their levels. This mini review examines and presents evidence supporting the use of KPMs as a relevant set of biomarkers for ALS, and highlights the criteria required to achieve a valid biomarker set for ALS.

Original languageEnglish
Article number1013
Pages (from-to)1-11
Number of pages11
JournalFrontiers in Neuroscience
Volume13
DOIs
Publication statusPublished - 20 Sep 2019

Bibliographical note

Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • amyotrophic lateral sclerosis
  • biomarker development
  • kynurenine pathway
  • motor neuron disease
  • neurodegeneration
  • neuroinflammation and neurodegeneration
  • tryptophan

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