Blunted Melatonin Circadian Rhythm in Parkinson's Disease: Express Bewilderment.

IF 2.9 3区医学 Q2 NEUROSCIENCES Neurotoxicity Research Pub Date : 2024-08-23 DOI:10.1007/s12640-024-00716-0

Areej Turkistani, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Walaa A Negm, Mostafa M Bahaa, Mostafa E Metawee, Gaber El-Saber Batiha

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Abstract

Melatonin (MTN) is a neuro-hormone released from the pineal gland. MTN secretion is regulated by different neuronal circuits, including the retinohypothalamic tract and suprachiasmatic nucleus (SCN), which are affected by light. MTN is neuroprotective in various neurodegenerative diseases, including Parkinson's disease (PD). MTN circulating level is highly blunted in PD. However, the underlying causes were not fully clarified. Thus, the present review aims to discuss the potential causes of blunted MTN levels in PD. Distortion of MTN circadian rhythmicity in PD patients causies extreme daytime sleepiness. The underlying mechanism for blunted MTN response may be due to reduction for light exposure, impairment of retinal light transmission, degeneration of circadian pacemaker and dysautonomia. In conclusion, degeneration of SCN and associated neurodegeneration together with neuroinflammation and activation of NF-κB and NLRP3 inflammasome, induce dysregulation of MTN secretion. Therefore, low serum MTN level reflects PD severity and could be potential biomarkers. Preclinical and clinical studies are suggested to clarify the underlying causes of low MTN in PD.

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帕金森病患者褪黑激素昼夜节律失调：表达困惑。

褪黑素（MTN）是松果体释放的一种神经激素。MTN 的分泌受不同神经元回路的调控，包括视网膜下丘脑束和丘脑上核（SCN），它们受到光的影响。MTN 对包括帕金森病（PD）在内的多种神经退行性疾病具有神经保护作用。帕金森病患者的 MTN 循环水平严重下降。然而，其根本原因尚未完全阐明。因此，本综述旨在讨论帕金森病中 MTN 水平降低的潜在原因。帕金森病患者 MTN 昼夜节律失调会导致白天极度嗜睡。MTN反应迟钝的潜在机制可能是由于光照减少、视网膜光传输受损、昼夜节律起搏器退化和自主神经功能障碍。总之，SCN 的退化和相关的神经变性，加上神经炎症和 NF-κB 及 NLRP3 炎性体的激活，导致 MTN 分泌失调。因此，低血清 MTN 水平反映了帕金森病的严重程度，可能成为潜在的生物标志物。建议开展临床前和临床研究，以明确 PD 中 MTN 水平低的根本原因。

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来源期刊

Neurotoxicity Research 医学-神经科学

CiteScore

7.70

自引率

5.40%

发文量

164

审稿时长

6-12 weeks

期刊介绍： Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.