Abstract

Activation of the kynurenine pathway (KP) of tryptophan metabolism results from chronic inflammation and is known to exacerbate progression of neurodegenerative disease. To gain insights into the links between inflammation, the KP and multiple sclerosis (MS) pathogenesis, we investigated the KP metabolomics profile of MS patients. Most significantly, we found aberrant levels of two key KP metabolites, kynurenic acid (KA) and quinolinic acid (QA). The balance between these metabolites is important as it determines overall excitotoxic activity at the N-methyl-D-Aspartate (NMDA) receptor. We also identified that serum KP metabolic signatures in patients can discriminate clinical MS subtypes with high sensitivity and specificity. A C5.0 Decision Tree classification model discriminated the clinical subtypes of MS with a sensitivity of 91%. After validation in another independent cohort, sensitivity was maintained at 85%. Collectively, our studies suggest that abnormalities in the KP may be associated with the switch from early-mild stage MS to debilitating progressive forms of MS and that analysis of KP metabolites in MS patient serum may have application as MS disease biomarkers.

Highlights

  • Has antioxidant activity, readily scavenging hydroxyl, superoxide anion and other free radicals[8]

  • A total of 59 participants consisting of 44 RRMS and 15 secondary progressive MS (SPMS) from Cohort 2 were included in this study

  • We evaluated the kynurenine pathway (KP) in multiple sclerosis (MS) in order to explore the links between inflammation, the KP and MS disease progression

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Summary

Introduction

Has antioxidant activity, readily scavenging hydroxyl, superoxide anion and other free radicals[8]. We examined the role of the KP in MS progression as it potentially links inflammation-induced activation of the KP10, the production of the glutamatergic (NMDA)-modulatory metabolites, KA and QA, to excitotoxic neurodegeneration[11,12,13]. This metabolic shift may explain why the inflammatory milieu in RRMS changes to a neurodegenerative one in SPMS and may even constitute a unique metabolic biomarker of MS progression. There are no biomarkers that can identify this transition[14], and a suitable biomarker would be useful for assessing patient prognosis and potentially new therapeutics

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