Could the kynurenine pathway be the key missing piece of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) complex puzzle?

Bahar Kavyani, Brett A. Lidbury, Richard Schloeffel, Paul R. Fisher, Daniel Missailidis, Sarah J. Annesley, Mona Dehhaghi, Benjamin Heng*, Gilles J. Guillemin*

*Corresponding author for this work

    Research output: Contribution to journalReview articlepeer-review

    8 Citations (Scopus)

    Abstract

    Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease with a substantial social and economic impact on individuals and their community. Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due to the unclear pathophysiology of the disease and consequently lack of prognostic biomarkers. To investigate pathophysiology of ME/CFS, several potential pathologic hallmarks have been investigated; however, these studies have failed to report a consistent result. These failures in introducing the underlying reason for ME/CFS have stimulated considering other possible contributing mechanisms such as tryptophan (TRP) metabolism and in particular kynurenine pathway (KP). KP plays a central role in cellular energy production through the production of nicotinamide adenine dinucleotide (NADH). In addition, this pathway has been shown to mediate immune response and neuroinflammation through its metabolites. This review, we will discuss the pathology and management of ME/CFS and provide evidence pertaining KP abnormalities and symptoms that are classic characteristics of ME/CFS. Targeting the KP regulation may provide innovative approaches to the management of ME/CFS.

    Original languageEnglish
    Article number412
    JournalCellular and Molecular Life Sciences
    Volume79
    Issue number8
    DOIs
    Publication statusPublished - Aug 2022

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