数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disorder characterized by the selective degeneration of upper and lower motor neurons, resulting in progressive muscle weakness, paralysis, and respiratory failure.
方法
Despite the availability of disease-modifying therapies, current treatment options provide only modest clinical benefits, highlighting the need for novel therapeutic strategies targeting multiple pathological mechanisms.
核心结论
Melatonin, a pleiotropic neuroprotective molecule with antioxidant, anti-inflammatory, and anti-apoptotic properties, has emerged as a promising candidate; however, its influence on glucagon-like peptide-1 (GLP-1)-associated neuroprotective signaling and related molecular events in ALS remains poorly understood.；Therefore, the present study investigated the neuroprotective efficacy of melatonin in a methylmercury (MTMR)-induced rat model of ALS and explored its effects on GLP-1-associated molecular alterations, neuroinflammation, oxidative stress, apoptosis, neurotransmitter homeostasis, demyelination, and neuronal injury.；Molecular docking analysis was performed to predict the interaction of melatonin with proteins implicated in ALS pathology.；Adult Wistar rats were exposed to MTMR (5 mg/kg, p.o.) for 21 days to induce ALS-like… ‖ 结论：Collectively, these findings demonstrate that melatonin substantially attenuates methylmercury-induced ALS-like neuropathology through coordinated modulation of multiple pathological processes associated with neurodegeneration.
局限
未能获取全文，具体设计细节、失访与统计学处理无法核验。
对本项目的价值
★★☆☆☆ 脑老化是最大未满足需求，也是终点最难量化的领域；biomarker 与认知读数选择最敏感。
原文题录
- 英文标题：Combined melatonin and edaravone therapy attenuates methylmercury-induced amyotrophic lateral sclerosis-like neurodegeneration through GLP-1 modulation and myelin preservation.
- 期刊与标识：Naunyn Schmiedebergs Arch Pharmacol · PMID 42946847 · DOI 10.1007/s00210-026-06009-x**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。