Baghcheghi Yousef, Razazpour Fateme, Mirzaee Faezeh, Dalfardi Mohammad, Pourfridoni Mohammad, Hedayati-Moghadam Mahdiyeh
Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, Iran.
Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran.
Mol Biol Rep. 2024 Dec 9;52(1):45. doi: 10.1007/s11033-024-10115-5.
Memory impairment is a critical challenge in neurodegenerative disorders, particularly in Alzheimer's disease, Parkinson's disease, and age-related cognitive decline. This research explores the molecular mechanisms by which curcumin, a polyphenolic compound derived from Curcuma longa, exerts neuroprotective effects that may ameliorate cognitive deficits associated with these conditions.
Evidence from both preclinical studies and emerging clinical trials indicates that curcumin enhances neuronal signaling and synaptic plasticity, primarily through the modulation of pathways such as NF-κB and PI3K/Akt. Specifically, curcumin has been shown to reduce neuroinflammation and oxidative stress, thereby promoting synaptic integrity and function. For instance, studies demonstrate that curcumin treatment increases the density of dendritic spines in the hippocampus, which correlates with improved spatial learning and memory performance in animal models. Despite promising findings, significant gaps remain in our understanding of curcumin's efficacy in humans. Most existing research is derived from animal studies, with limited large-scale clinical trials to substantiate its therapeutic potential. Furthermore, challenges such as curcumin's low bioavailability and inconsistencies in dosing complicate its clinical application. This review underscores the need for future research focused on enhancing curcumin's bioavailability, establishing optimal dosages, and conducting comprehensive human trials to validate its effectiveness. By addressing these issues, we aim to clarify curcumin's role as a potential therapeutic agent for memory impairment in neurodegenerative disorders, paving the way for innovative treatment strategies.
记忆障碍是神经退行性疾病中的一项关键挑战，尤其是在阿尔茨海默病、帕金森病以及与年龄相关的认知衰退中。本研究探索了姜黄素（一种从姜黄中提取的多酚类化合物）发挥神经保护作用的分子机制，这种作用可能改善与这些病症相关的认知缺陷。
临床前研究和新兴临床试验的证据均表明，姜黄素主要通过调节核因子κB（NF-κB）和磷脂酰肌醇-3-激酶/蛋白激酶B（PI3K/Akt）等信号通路来增强神经元信号传导和突触可塑性。具体而言，姜黄素已被证明可减轻神经炎症和氧化应激，从而促进突触完整性和功能。例如，研究表明姜黄素治疗可增加海马体中树突棘的密度，这与动物模型中空间学习和记忆能力的改善相关。尽管有这些有前景的发现，但我们对姜黄素在人体中的疗效仍存在重大认知差距。现有的大多数研究来自动物实验，大规模临床试验有限，难以证实其治疗潜力。此外，姜黄素的低生物利用度和剂量不一致等问题使其临床应用变得复杂。本综述强调了未来研究的必要性，即专注于提高姜黄素的生物利用度、确定最佳剂量，并进行全面的人体试验以验证其有效性。通过解决这些问题，我们旨在阐明姜黄素作为神经退行性疾病记忆障碍潜在治疗药物的作用，为创新治疗策略铺平道路。
