The role of microRNAs in neurodegenerative diseases: a review

MicroRNAs (miRNAs) are non-coding RNAs which are essential post-transcriptional gene regulators in various neuronal degenerative diseases and playact a key role in these physiological progresses. Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, multiple sclerosis, and, stroke, are seriously threats to the life and health of all human health and life kind. Recently, various studies have reported that some various miRNAs can regulate the development of neurodegenerative diseases as well as act as biomarkers to predict these neuronal diseases conditions. Endogenic miRNAs such as miR-9, the miR-29 family, miR-15, and the miR-34 family are generally dysregulated in animal and cell models. They are involved in regulating the physiological and biochemical processes in the nervous system by targeting regulating different molecular targets and influencing a variety of pathways. Additionally, exogenous miRNAs derived from homologous plants and defined as botanmin, such as miR2911 and miR168, can be taken up and transferred by other species to be and then act analogously to endogenic miRNAs to regulate the physiological and biochemical processes. This review summarizes the mechanism and principle of miRNAs in the treatment of some neurodegenerative diseases, as well as discusses several types of miRNAs which were the most commonly reported in diseases. These miRNAs could serve as a study provided some potential biomarkers in neurodegenerative diseases might be an ideal and/or therapeutic targets for neurodegenerative diseases. Finally, the role accounted of the prospective exogenous miRNAs involved in mammalian diseases is described. GRAPHICAL ABSTRACT: 1. Listing a large number of neural-related miRNAs and sorting out their pathways. 2. Classify and sort miRNAs according to their mechanism of action. 3. Demonstrating the effects of up-regulation or down-regulation of each miRNAs on the nervous system. [Image: see text]