Gupta Babita, Malviya Rishabha, Sundram Sonali, Sridhar Sathvik Belagodu, Singh Deependra Pratap
Department of Pharmacy, School of Medical and Allied Sciences, Galgotias University, Greater Noida, India.
Department of Clinical Pharmacy & Pharmacology, RAK College of Pharmacy, RAK Medical Health Sciences University, Ras Al Khaimah, United Arab Emirates.
Curr Top Med Chem. 2025 Jan 29. doi: 10.2174/0115680266327614241121050448.
Alzheimer's Disease (AD), a progressive neurodegenerative disorder, is characterized by the accumulation of neurofibrillary tangles and β-amyloid plaques, leading to a decline in cognitive function. AD is characterized by tau protein hyperphosphorylation and extracellular β-amyloid accumulation. Even after much research, there are still no proven cures for AD. The neuroprotective, anti-inflammatory, and antioxidant qualities of melatonin, a hormone mostly produced by the pineal gland, have drawn interest as a possible treatment option for AD. This study looks at new evidence that suggests melatonin overexpression to be a promising therapy option for AD. Melatonin levels naturally decline with age and decrease more significantly in individuals with AD, worsening neurodegenerative processes. Melatonin has therapeutic potential as it inhibits Aβ formation, prevents amyloid fibril extension through structure-dependent interactions, and protects neurons from Aβ-induced toxicity. Melatonin promotes neurogenesis, which is decreased in AD, suggesting it may treat the disease's many pathologies. The review emphasizes the importance of melatonin's mechanisms of action, including its capacity to reduce neuroinflammation, regulate mitochondrial function, scavenge free radicals, and influence apoptotic pathways. As research into AD continues, this article provides a forward-looking perspective on how future studies could leverage melatonin's multifaceted neuroprotective properties to develop more effective treatments for AD.
阿尔茨海默病（AD）是一种进行性神经退行性疾病，其特征是神经原纤维缠结和β-淀粉样蛋白斑块的积累，导致认知功能下降。AD的特征是tau蛋白过度磷酸化和细胞外β-淀粉样蛋白积累。即使经过大量研究，AD仍然没有经过证实的治愈方法。褪黑素是一种主要由松果体产生的激素，其神经保护、抗炎和抗氧化特性引起了人们的兴趣，有可能成为AD的一种治疗选择。本研究探讨了新的证据，表明褪黑素过表达是一种有前途的AD治疗选择。褪黑素水平会随着年龄的增长而自然下降，在AD患者中下降得更明显，从而加剧神经退行性过程。褪黑素具有治疗潜力，因为它能抑制Aβ的形成，通过结构依赖性相互作用防止淀粉样纤维延伸，并保护神经元免受Aβ诱导的毒性。褪黑素能促进神经发生，而神经发生在AD中会减少，这表明它可能治疗该疾病的多种病理状况。该综述强调了褪黑素作用机制的重要性，包括其减少神经炎症、调节线粒体功能、清除自由基和影响细胞凋亡途径的能力。随着对AD研究的不断深入，本文提供了一个前瞻性的视角，即未来的研究如何利用褪黑素多方面的神经保护特性来开发更有效的AD治疗方法。
