Citation

Tan LSY, Francis HM, Lim CK. Brain Behav. Immun. Health 2021; 12.

Copyright

(Copyright © 2021, Elsevier Publishing)

DOI

10.1016/j.bbih.2021.100201

PMID

unavailable

Abstract

The metabolism of tryptophan through the kynurenine pathway (KP) has been increasingly recognised in contributing to disease progression in the autoimmune and inflammatory disease multiple sclerosis (MS). In this review, the roles of inflammation and the KP are recontextualised to better understand the aetiology of the neuropsychiatric symptoms (depression, postpartum depression, suicidality, fatigue and cognitive dysfunction) in MS. These symptoms will be discussed in the context of cytokine-induced sickness behaviours, KP activation and levels of neurotoxicity and neuroprotection in MS. In particular, there will be emphasis on how neuropsychiatric symptoms in MS occur against the shared background of inflammation and KP dysregulation. The discourse of this review aims to promote future research in elucidating KP mechanisms in MS that would inevitably lead to more targeted treatment options for neuropsychiatric symptoms and disease progression. © 2021 The Authors

Language: en

Keywords

human; Depression; Review; Fatigue; depression; Multiple sclerosis; suicide attempt; suicidal behavior; pathogenesis; kynurenine; serotonin; mental disease; antidepressant agent; disease association; dysthymia; cognitive defect; priority journal; neurotoxicity; Alzheimer disease; nonhuman; disease exacerbation; symptom; illness behavior; melatonin; tryptophan; multiple sclerosis; cytokine; Cognitive dysfunction; protein function; diet supplementation; neuroprotection; diet therapy; postnatal depression; nerve degeneration; neuromodulation; tryptophan metabolism; nervous system inflammation; Kynurenine pathway; Neuroinflammation