Journal
FRONTIERS IN NEUROSCIENCE
Volume 15, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2021.658202
Keywords
multiple sclerosis; kynurenine; neurofilaments; quinolinic acid; glutamate excitotoxicity; mitochondrial dysfunction; neuro-axonal damage; oxidative stress
Categories
Funding
- Ministry of Human Capacities [GINOP-2.3.2-15-2016-00034, EFOP-3.6.1-16-2016-00008, 20391-3/2018/FEKUSTRAT]
- TKP 2020 Thematic Excellence Program [NKFIH-1279-2/2020]
- New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund [UNKP-20-3, EFOP 3.6.3-VEKOP-16-2017-00009]
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The kynurenine pathway is involved in the pathogenesis of multiple sclerosis, with dysregulation and upregulated levels contributing to neuro-axonal damage and degeneration. Neurofilaments serve as reliable biomarkers for neuro-axonal damage severity and treatment response in multiple sclerosis. There is increasing evidence of a connection between molecules in the kynurenine metabolic pathway and changes in neurofilament concentrations, suggesting its potential as an important biomarker for disease progression.
Multiple sclerosis is an autoimmune, demyelinating, and neurodegenerative disease of the central nervous system. In recent years, it has been proven that the kynurenine system plays a significant role in the development of several nervous system disorders, including multiple sclerosis. Kynurenine pathway metabolites have both neurotoxic and neuroprotective effects. Moreover, the enzymes of the kynurenine pathway play an important role in immunomodulation processes, among others, as well as interacting with neuronal energy balance and various redox reactions. Dysregulation of many of the enzymatic steps in kynurenine pathway and upregulated levels of these metabolites locally in the central nervous system, contribute to the progression of multiple sclerosis pathology. This process can initiate a pathogenic cascade, including microglia activation, glutamate excitotoxicity, chronic oxidative stress or accumulated mitochondrial damage in the axons, that finally disrupt the homeostasis of neurons, leads to destabilization of neuronal cell cytoskeleton, contributes to neuro-axonal damage and neurodegeneration. Neurofilaments are good biomarkers of the neuro-axonal damage and their level reliably indicates the severity of multiple sclerosis and the treatment response. There is increasing evidence that connections exist between the molecules generated in the kynurenine metabolic pathway and the change in neurofilament concentrations. Thus the alterations in the kynurenine pathway may be an important biomarker of the course of multiple sclerosis. In our present review, we report the possible relationship and connection between neurofilaments and the kynurenine system in multiple sclerosis based on the available evidences.
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