Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Neuroscience & Pharmacology, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Neurology, Departments of School of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Public Health Department of Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Neuroscience & Pharmacology, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Neurology, Departments of School of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Public Health Department of Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA; Department of Speech, Language and Hearing Sciences, School Health Professions, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Ageing Res Rev. 2022 Jan;73:101529. doi: 10.1016/j.arr.2021.101529. Epub 2021 Nov 20.
Alzheimer's disease (AD) is the most common cause of dementia and is currently one of the biggest public health concerns in the world. Mitochondrial dysfunction in neurons is one of the major hallmarks of AD. Emerging evidence suggests that mitochondrial miRNAs potentially play important roles in the mitochondrial dysfunctions, focusing on synapse in AD progression. In this meta-analysis paper, a comprehensive literature review was conducted to identify and discuss the (1) role of mitochondrial miRNAs that regulate mitochondrial and synaptic functions; (2) the role of various factors such as mitochondrial dynamics, biogenesis, calcium signaling, biological sex, and aging on synapse and mitochondrial function; (3) how synapse damage and mitochondrial dysfunctions contribute to AD; (4) the structure and function of synapse and mitochondria in the disease process; (5) latest research developments in synapse and mitochondria in healthy and disease states; and (6) therapeutic strategies that improve synaptic and mitochondrial functions in AD. Specifically, we discussed how differences in the expression of mitochondrial miRNAs affect ATP production, oxidative stress, mitophagy, bioenergetics, mitochondrial dynamics, synaptic activity, synaptic plasticity, neurotransmission, and synaptotoxicity in neurons observed during AD. However, more research is needed to confirm the locations and roles of individual mitochondrial miRNAs in the development of AD.
阿尔茨海默病（AD）是痴呆症最常见的病因，也是目前全球最大的公共卫生关注点之一。神经元中线粒体功能障碍是 AD 的主要标志之一。新出现的证据表明，线粒体 miRNA 可能在线粒体功能障碍中发挥重要作用，特别是在 AD 进展中的突触中。在这篇荟萃分析论文中，进行了全面的文献综述，以确定和讨论：（1）调节线粒体和突触功能的线粒体 miRNA 的作用；（2）线粒体动力学、生物发生、钙信号、生物性别和衰老等各种因素对突触和线粒体功能的影响；（3）突触损伤和线粒体功能障碍如何导致 AD；（4）突触和线粒体在疾病过程中的结构和功能；（5）健康和疾病状态下突触和线粒体的最新研究进展；以及（6）改善 AD 中突触和线粒体功能的治疗策略。具体而言，我们讨论了在 AD 中观察到的线粒体 miRNA 表达差异如何影响神经元中的 ATP 产生、氧化应激、自噬、生物能学、线粒体动力学、突触活动、突触可塑性、神经传递和突触毒性。然而，需要更多的研究来证实单个线粒体 miRNA 在 AD 发展中的位置和作用。
