Reddy P Hemachandra, Tonk Sahil, Kumar Subodh, Vijayan Murali, Kandimalla Ramesh, Kuruva Chandra Sekhar, Reddy Arubala P
Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, United States.
Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
Biochem Biophys Res Commun. 2017 Feb 19;483(4):1156-1165. doi: 10.1016/j.bbrc.2016.08.067. Epub 2016 Aug 12.
Currently, 5.4 million Americans suffer from AD, and these numbers are expected to increase up to 16 million by 2050. Despite tremendous research efforts, we still do not have drugs or agents that can delay, or prevent AD and its progression, and we still do not have early detectable biomarkers for AD. Multiple cellular changes have been implicated in AD, including synaptic damage, mitochondrial damage, production and accumulation of Aβ and phosphorylated tau, inflammatory response, deficits in neurotransmitters, deregulation of the cell cycle, and hormonal imbalance. Research into AD has revealed that miRNAs are involved in each of these cellular changes and interfere with gene regulation and translation. Recent discoveries in molecular biology have also revealed that microRNAs play a major role in post-translational regulation of gene expression. The purpose of this article is to review research that has assessed neuroprotective and neurodegenerative characteristics of microRNAs in brain samples from AD transgenic mouse models and patients with AD.
目前，540万美国人患有阿尔茨海默病（AD），预计到2050年这一数字将增至1600万。尽管进行了大量研究，但我们仍然没有能够延缓或预防AD及其进展的药物或制剂，也没有可早期检测的AD生物标志物。AD涉及多种细胞变化，包括突触损伤、线粒体损伤、β淀粉样蛋白（Aβ）和磷酸化tau蛋白的产生与积累、炎症反应、神经递质缺乏、细胞周期失调以及激素失衡。对AD的研究表明，微小RNA（miRNA）参与了上述每一种细胞变化，并干扰基因调控和翻译过程。分子生物学的最新发现还表明，微小RNA在基因表达的翻译后调控中起主要作用。本文旨在综述评估AD转基因小鼠模型和AD患者脑样本中微小RNA的神经保护和神经退行性特征的研究。
