Melatonin as an inducing factor for multiple sclerosis

Em, Kuklina

doi:10.17116/jnevro201611651102-105

Cited by 1 publication

(1 citation statement)

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“…In addition, case studies reported that using picoTesla magnetic fields improved disability in MS patients, which was accompanied by a reduction in melatonin levels, possibly by downregulation of its immunoenhancing effects 48 . This deleterious role of melatonin in MS was also proposed by Kuklina et al 49 and Constantinescu et al 2 Moreover, in cultured human monocytes, melatonin showed a high immunoenhancing effect by activating these monocytes and increasing IL-1α and IL-1β 45 . Furthermore, another study showed the potential of melatonin to increase IFN-γ, IL-2, and IL-6 in circulating human CD4 + cells through the melatonin nuclear receptor 50 .…”

Section: Discussionsupporting

confidence: 63%

Inhibiting nighttime melatonin and boosting cortisol increase patrolling monocytes, phagocytosis, and myelination in a murine model of multiple sclerosis

et al. 2023

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Conflicting results on melatonin synthesis in multiple sclerosis (MS) have been reported due to variabilities in patient lifestyles, which are not considered when supplementing melatonin. Since melatonin acts through its receptors, we identified melatonin receptors in oligodendrocytes (OLs) in the corpus callosum, where demyelination occurs; the subventricular zone, where neural stem/progenitor cells (NSPCs) are located; and the choroid plexus, which functions as a blood-cerebrospinal fluid barrier. Moreover, using chimeric mice, resident macrophages were found to express melatonin receptors, whereas bone marrow-derived macrophages lost this expression in the demyelinated brain. Next, we showed that cuprizone-fed mice, which is an MS model, tended to have increased melatonin levels. While we used different approaches to alter the circadian rhythm of melatonin and cortisol, only the constant light approach increased NSPC proliferation and differentiation to oligodendrocyte precursor cells (OPCs), OPCs maturation to OLs and recruitment to the site of demyelination, the number of patrolling monocytes, and phagocytosis. In contrast, constant darkness and exogenous melatonin exacerbated these events and amplified monocyte infiltration. Therefore, melatonin should not be considered a universal remedy, as is currently claimed. Our data emphasize the importance of monitoring melatonin/cortisol oscillations in each MS patient by considering diet and lifestyle to avoid melatonin overdose.

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