Rahman Md Ataur, Rahman Md Hasanur, Biswas Partha, Hossain Md Shahadat, Islam Rokibul, Hannan Md Abdul, Uddin Md Jamal, Rhim Hyewhon
Center for Neuroscience, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Global Biotechnology & Biomedical Research Network (GBBRN), Department of Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia 7003, Bangladesh.
Antioxidants (Basel). 2020 Dec 28;10(1):23. doi: 10.3390/antiox10010023.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a decline in cognitive function and neuronal damage. Although the precise pathobiology of AD remains elusive, accumulating evidence suggests that mitochondrial dysfunction is one of the underlying causes of AD. Mutations in mitochondrial or nuclear DNA that encode mitochondrial components may cause mitochondrial dysfunction. In particular, the dysfunction of electron transport chain complexes, along with the interactions of mitochondrial pathological proteins are associated with mitochondrial dysfunction in AD. Mitochondrial dysfunction causes an imbalance in the production of reactive oxygen species, leading to oxidative stress (OS) and vice versa. Neuroinflammation is another potential contributory factor that induces mitochondrial dysfunction. Phytochemicals or other natural compounds have the potential to scavenge oxygen free radicals and enhance cellular antioxidant defense systems, thereby protecting against OS-mediated cellular damage. Phytochemicals can also modulate other cellular processes, including autophagy and mitochondrial biogenesis. Therefore, pharmacological intervention via neuroprotective phytochemicals can be a potential strategy to combat mitochondrial dysfunction as well as AD. This review focuses on the role of phytochemicals in mitigating mitochondrial dysfunction in the pathogenesis of AD.
阿尔茨海默病(AD)是一种进行性神经退行性疾病,其特征为认知功能下降和神经元损伤。尽管AD的确切病理生物学机制仍不清楚,但越来越多的证据表明线粒体功能障碍是AD的潜在病因之一。编码线粒体成分的线粒体DNA或核DNA突变可能导致线粒体功能障碍。特别是,电子传递链复合物的功能障碍以及线粒体病理蛋白的相互作用与AD中的线粒体功能障碍有关。线粒体功能障碍会导致活性氧生成失衡,进而导致氧化应激(OS),反之亦然。神经炎症是另一个诱发线粒体功能障碍的潜在因素。植物化学物质或其他天然化合物具有清除氧自由基和增强细胞抗氧化防御系统的潜力,从而防止OS介导的细胞损伤。植物化学物质还可以调节其他细胞过程,包括自噬和线粒体生物发生。因此,通过具有神经保护作用的植物化学物质进行药物干预可能是对抗线粒体功能障碍以及AD的潜在策略。本综述重点关注植物化学物质在减轻AD发病机制中线粒体功能障碍方面的作用。