Neuroprotective effects of melatonin in neurodegenerative and autoimmune central nervous system diseases.

Autoimmune diseases of the nervous system Circadian rhythm Melatonin Neurodegenerative diseases Neuroprotection

Journal

Encephalitis (Seoul, Korea)

ISSN: 2734-1461

Titre abrégé: Encephalitis

Pays: Korea (South)

ID NLM: 9918592381006676

Informations de publication

Date de publication:
Apr 2023

Historique:

received: 11 10 2022

revised: 24 11 2022

accepted: 15 12 2022

medline: 20 7 2023

pubmed: 20 7 2023

entrez: 20 7 2023

Statut: ppublish

Résumé

The suprachiasmatic nucleus (SCN) in the anterior hypothalamus is the major circadian pacemaker in humans. Melatonin is a key hormone secreted by the pineal gland in response to darkness. Light-induced stimuli are transmitted along the retinohypothalamic tract to the SCN. Activation of the SCN inhibits the production of melatonin by the pineal gland through a complex neural pathway passing through the superior cervical ganglion. Accordingly, when light is unavailable, the pineal gland secretes melatonin. The circadian rhythm modulates sleep-wake cycles as well as many physiological functions of the endocrine system, including core body temperature, pulse rate, oxygen consumption, hormone levels, metabolism, and gastrointestinal function. In neurodegenerative disorders, the sleep-wake cycle is disrupted and circadian regulation is altered, which accelerates disease progression, further disrupting circadian regulation and setting up a vicious cycle. Melatonin plays a critical role in the regulation of circadian rhythms and is a multifunctional pleiotropic agent with broad neuroprotective effects in neurodegenerative disorders, viral or autoimmune diseases, and cancer. In this review, I discuss the neuroprotective functions of melatonin in circadian regulation and its roles in promoting anti-inflammatory activity, enhancing immune system functions, and preventing alterations in glucose metabolism and mitochondrial dysfunction in neurodegenerative disorders and autoimmune central nervous system diseases.

Identifiants

DOI: 10.47936/encephalitis.2022.00094 PMID: 37469673 PMC: PMC10295826

pubmed: 37469673

doi: 10.47936/encephalitis.2022.00094

pii: encephalitis-2022-00094

pmc: PMC10295826

doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

44-53

Informations de copyright

Déclaration de conflit d'intérêts

Conflicts of Interest No potential conflict of interest relevant to this article was reported.

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