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

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...

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Published in:Cellular and molecular life sciences : CMLS 2022-08, Vol.79 (8), p.412-412, Article 412
Main Authors: Kavyani, Bahar, Lidbury, Brett A., Schloeffel, Richard, Fisher, Paul R., Missailidis, Daniel, Annesley, Sarah J., Dehhaghi, Mona, Heng, Benjamin, Guillemin, Gilles J.
Format: Article
Language:English
Subjects:
Abnormalities
Adenine
Biochemistry
Biomarkers
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cellular manufacture
Chronic fatigue syndrome
Economic impact
Encephalomyelitis
Fatigue
Fatigue Syndrome, Chronic - diagnosis
Fatigue Syndrome, Chronic - therapy
Humans
Immune response
Impact analysis
Inflammation
Kynurenine
Life Sciences
Metabolites
NAD
NADH
Nicotinamide
Nicotinamide adenine dinucleotide
Pathophysiology
Review
Signs and symptoms
Tryptophan
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Summary: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.
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-022-04380-5