Abstract
Exploring the microRNAs and aptamers for their therapeutic role as biological drugs has expanded the horizon of its applicability against various human diseases, explicitly targeting the genetic materials. RNA-based therapeutics are widely being explored for the treatment and diagnosis of multiple diseases, including neurodegenerative disorders (NDD). Latter includes microRNA, aptamers, ribozymes, and small interfering RNAs (siRNAs), which control the gene expression mainly at the transcriptional strata. One RNA transcript translates into different protein types; hence, therapies targeted at the transcriptional sphere may have prominent and more extensive effects than alternative therapeutics. Unlike conventional gene therapy, RNAs, upon delivery, can either altogether abolish or alter the synthesis of the protein of interest, therefore, regulating their activities in a controlled and diverse manner. NDDs like Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, multiple sclerosis, Prion disease, and others are characterized by deposition of misfolded protein such as amyloid-ß, tau, α-synuclein, huntingtin and prion proteins. Neuroinflammation, one of the perquisites for neurodegeneration, is induced during neurodegenerative pathogenesis. In this review, we discuss microRNAs and aptamers' role as two different RNA-based approaches for their unique ability to regulate protein production at the transcription level, hence offering many advantages over other biologicals. The microRNA acts either by alleviating the malfunctioning RNA expression or by working as a replacement to lost microRNA. On the contrary, aptamer act as a chemical antibody and forms an aptamer-target complex.
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Islauddin Khan, including other authors, is thankful to the Department of Pharmacology and Toxicology, NIPER Hyderabad, Department of Pharmaceuticals, Ministry of Chemicals and Fertilizers Govt. of India.
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Khan, I., Preeti, K., Fernandes, V. et al. Role of MicroRNAs, Aptamers in Neuroinflammation and Neurodegenerative Disorders. Cell Mol Neurobiol 42, 2075–2095 (2022). https://doi.org/10.1007/s10571-021-01093-4
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DOI: https://doi.org/10.1007/s10571-021-01093-4