Abstract
MicroRNAs (miRNAs) are a class of short, non-coding, regulatory RNA molecules that function as post transcriptional regulators of gene expression. Altered expression of multiple miRNAs was found to be extensively involved in the pathogenesis of different neurological disorders including Alzheimer’s disease, Parkinson’s disease, stroke, epilepsy, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington’s disease. miRNAs are implicated in the pathogenesis of excitotoxicity, apoptosis, oxidative stress, inflammation, neurogenesis, angiogenesis, and blood–brain barrier protection. Consequently, miRNAs can serve as biomarkers for different neurological disorders. In recent years, advances in the miRNA field led to identification of potentially novel prospects in the development of new therapies for incurable CNS disorders. MiRNA-based therapeutics include miRNA mimics and inhibitors that can decrease or increase the expression of target genes. Better understanding of the mechanisms by which miRNAs are implicated in the pathogenesis of neurological disorders may provide novel targets to researchers for innovative therapeutic strategies.
Highlights
MiRNAs are a class of short, non-coding RNA molecules that contain 19-24 nucleotides
MiRNA are implicated in the pathogenesis of excitotoxicity, apoptosis, oxidative stress, inflammation, neurogenesis, angiogenesis, and blood–brain barrier protection [3]
It is not surprising that miRNAs have emerged as key regulators of pathophysiology of different neurological disorders including Alzheimer’s disease, Parkinson’s disease, stroke, epilepsy, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington’s disease [4]
Summary
MiRNAs are a class of short, non-coding RNA molecules that contain 19-24 nucleotides. MiRNA-based therapeutics include miRNA mimics and inhibitors that can decrease or increase the expression of target genes [8]. Blood brain barrier/blood spinal cord barrier (BBB/BSCB) protection The inflammatory cascade following damage to the BBB or the BSCB can be modulated by some miRNAs. Downregulating miR-150 alleviated BBB disruption after ischemic stroke through increasing claudin-5 and. Some miRNAs were reported to influences molecular and cellular pathways implicated in epilepsy, including oxidative stress, inflammation, immune responses, cell differentiation, migration, and proliferation [49–51] (Fig. 4). Targeting these miRNAs is a challenge for future strategies for anti-epileptogenesis therapy. Blocking the modulation of these miRNAs can completely abolish the neuroprotective effects of these agents against CNS injuries (Fig. 6)
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