Melatonin: A review of its potential functions and effects on neurological diseases

Gunata, Mehmet; Parlakpınar, Hakan; Acet, Hacı Ahmet

doi:10.1016/j.neurol.2019.07.025

Cited by 125 publications

(98 citation statements)

References 190 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Melatonin is a neuroendocrine hormone, and decreased melatonin secretion is associated with the progression of neurodegenerative diseases typified by neuronal death, such as AD, Parkinson's disease (PD), Huntington's disease (HD), and stroke. 44,45 Melatonin plays a critical role in controlling inflammation, oxidative stress, autophagy, mitochondrial homeostasis, apoptosis, calcium excitotoxicity, and pivotal signaling pathways in neurodegeneration. 25 However, the effect of melatonin on DM-induced neuronal death is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

View full text Add to dashboard Cite

Diabetes mellitus (DM) patients are at a higher risk of developing brain injury characterized by neuronal death. Melatonin, a hormone produced by the pineal gland, exerts neuroprotective effects against brain damage. However, the effect of melatonin on diabetes‐induced brain injury has not been elucidated. This study was to evaluate the role of melatonin against neuronal death in DM and to elucidate the underlying mechanisms. Herein, we found that melatonin administration significantly alleviated the neuronal death in both streptozotocin (STZ)‐induced diabetic mice and high glucose (HG)‐treated neuronal cells. Melatonin inhibited neuronal pyroptosis and excessive autophagy, as evidenced by decreased levels of NLRP3, cleaved caspase‐1, GSDMD‐N, IL‐1β, LC3, Beclin1, and ATG12 both in vivo and in vitro. MicroRNA‐214‐3p (miR‐214‐3p) was decreased in DM mice and HG‐treated cells, and such a downregulation was corrected by melatonin, which was accompanied by repression of caspase‐1 and ATG12. Furthermore, downregulation of miR‐214‐3p abrogated the anti‐pyroptotic and anti‐autophagic actions of melatonin in vitro. Our results indicate that melatonin exhibits a neuroprotective effect by inhibiting neuronal pyroptosis and excessive autophagy through modulating the miR‐214‐3p/caspase‐1 and miR‐214‐3p/ATG12 axes, respectively, and it might be a potential agent for the treatment of brain damage in the setting of DM.

show abstract

Section: Discussionmentioning

confidence: 99%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

View full text Add to dashboard Cite

show abstract

“…Although melatonin displays almost no side effects, even with high-dose and long-term administration, in patients in most clinical studies, some adverse reactions of melatonin—including drowsiness, fever, headache, vomiting, thrombosis, drowsiness, hyperkinesia or restless leg syndrome—may occur [ 10 , 203 ]. Therefore, the use of melatonin should be considered seriously with respect to the dosage and duration.…”

Section: Discussionmentioning

confidence: 99%

“…Melatonin is mainly produced from pinealocytes in the pineal grand and also synthesized in other organs such as the bone marrow, retina, skin and gastrointestinal tract (GIT). The whole procedure of melatonin biosynthesis occurs principally in four steps including hydroxylation, decarboxylation, acetylation and methylation ( Figure 1 ) [ 2 , 10 ]. Firstly, L-tryptophan is turned into 5-hydroxytryptophan by tryptophan hydroxylase with the stimulus of dark.…”

Section: Biosynthesis Of Melatoninmentioning

confidence: 99%

“…Cumulative evidence has suggested that melatonin has preventive and therapeutic effects on many neurodegenerative disorders [ 6 , 37 ]. Neurodegenerative diseases have been reported to share common pathophysiological features, such as disruption of the circadian rhythm, increased oxidative stress, neuroinflammation, neuronal loss, autophagic deficiency and mitochondrial dysfunction [ 10 , 38 ]. The level of melatonin decreases in elderly individuals, which may contribute to the development of neurodegenerative disease [ 39 , 40 ].…”

Section: Effects and Molecular Mechanisms Of Melatonin In Neurodegmentioning

confidence: 99%

See 1 more Smart Citation

Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases

2020

View full text Add to dashboard Cite

Neurodegenerative diseases are the second most common cause of death and characterized by progressive impairments in movement or mental functioning in the central or peripheral nervous system. The prevention of neurodegenerative disorders has become an emerging public health challenge for our society. Melatonin, a pineal hormone, has various physiological functions in the brain, including regulating circadian rhythms, clearing free radicals, inhibiting biomolecular oxidation, and suppressing neuroinflammation. Cumulative evidence indicates that melatonin has a wide range of neuroprotective roles by regulating pathophysiological mechanisms and signaling pathways. Moreover, melatonin levels are decreased in patients with neurodegenerative diseases. In this review, we summarize current knowledge on the regulation, molecular mechanisms and biological functions of melatonin in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, vascular dementia and multiple sclerosis. We also discuss the clinical application of melatonin in neurodegenerative disorders. This information will lead to a better understanding of the regulation of melatonin in the brain and provide therapeutic options for the treatment of various neurodegenerative diseases.

show abstract

“…All this process guides the synthesis of melatonin. Chemically, melatonin is an indolamine, derived from the amino acid tryptophan, and has lipophilic properties due to two functional groups the 5‐methoxy group and the N ‐acetyl side chain (Gunata et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Two neuroendocrine G protein‐coupled receptor molecules, somatostatin and melatonin: Physiology of signal transduction and therapeutic perspectives

Costanzi

Simioni

Conti

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

Recent studies have shown that G protein‐coupled receptors (GPCRs), the largest signal‐conveying receptor family, are targets for mutations occurring frequently in different cancer types. GPCR alterations associated with cancer development represent significant challenges for the discovery and the advancement of targeted therapeutics. Among the different molecules that can activate GPCRs, we focused on two molecules that exert their biological actions regulating many typical features of tumorigenesis such as cellular proliferation, survival, and invasion: somatostatin and melatonin. The modulation of signaling pathways, that involves these two molecules, opens an interesting scenario for cancer therapy, with the opportunity to act at different molecular levels. Therefore, the aim of this review is the analysis of the biological activity and the therapeutic potential of somatostatin and melatonin, displaying a high affinity for GPCRs, that interfere with cancer development and maintenance.

show abstract

Melatonin: A review of its potential functions and effects on neurological diseases

Cited by 125 publications

References 190 publications

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases

Two neuroendocrine G protein‐coupled receptor molecules, somatostatin and melatonin: Physiology of signal transduction and therapeutic perspectives

Contact Info

Product

Resources

About