Non-coding RNAs (ncRNAs) and neuroinflammation: implications for neurological disorders Non-coding RNAs (ncRNAs) are crucial regulators in various biological processes, challenging the traditional view that RNA functions only as a template for protein synthesis. Over the past two decades, research has shown that ncRNAs play essential roles in developmental timing, hormone regulation, chromosomal inactivation, and maintaining normal cellular circuitry that prevents chronic disease. ncRNAs, including miRNAs, lncRNAs, and circRNAs, have been identified as endogenous genetic regulators of mRNA abundance and control the expression and activity of other ncRNAs. miRNAs are particularly important in regulating gene expression and inflammatory responses, and have been implicated in various neurological disorders such as Parkinson's, ALS, epilepsy, Alzheimer's, and Huntington's. miRNAs regulate cell-signaling regulatory networks at the post-transcriptional level, resulting in controlled cellular development responsive to extracellular stimuli. miRNAs also control the expression of genetic outputs during neuronal development. This neuronal cellular process is tightly regulated and tuned by acute and/or chronic inflammatory cues that, when disrupted, result in the onset of various neurological disorders. This review highlights miRNAs that modulate the neuroinflammatory state within the central nervous system and elucidates the underlying mechanisms that promote or abrogate excessive inflammatory signaling as these biomolecules may become new therapeutic targets in the treatment of chronic neurological disorders such as epilepsy, ALS, Parkinson's, Alzheimer's, and Huntington's. miRNAs are small ncRNAs that modulate gene expression by binding to complementary sequences predominantly within the 3'UTR of target mRNAs. miRNAs are endogenously expressed in the genome and transcribed in the nucleus by RNA polymerase II/III. The resulting primary miRNA (pri-miRNA) transcript is unique in that the pri-miRNA folds creating hairpin bulges similar to tRNA, which is recognized by the RNaseIII enzyme DROSHA. Pri-miRNAs can originate from large intergenic regions of the genome, as well as from intronic regions, and sometimes are polycistronic and contain multiple mature miRNA sequences. The biogenesis of miRNAs involves a series of enzymatic cleavages and processing steps, resulting in the production of mature miRNA duplexes that can be incorporated into RISC complexes to regulate gene expression. miRNAs play a significant role in the activation or suppression of neuroinflammation by controlling the abundance of central mediators of NLRP3 priming and/or activation of the inflammasome. miR-155, for example, regulates the activity of NF-κB, a major protein complex that controls DNA transcription and cytokine production, supports maturation of dendritic cells, promotes recruitment of neutrophils, stimulates M1 polarization of macrophage and microglial cellsNon-coding RNAs (ncRNAs) and neuroinflammation: implications for neurological disorders Non-coding RNAs (ncRNAs) are crucial regulators in various biological processes, challenging the traditional view that RNA functions only as a template for protein synthesis. Over the past two decades, research has shown that ncRNAs play essential roles in developmental timing, hormone regulation, chromosomal inactivation, and maintaining normal cellular circuitry that prevents chronic disease. ncRNAs, including miRNAs, lncRNAs, and circRNAs, have been identified as endogenous genetic regulators of mRNA abundance and control the expression and activity of other ncRNAs. miRNAs are particularly important in regulating gene expression and inflammatory responses, and have been implicated in various neurological disorders such as Parkinson's, ALS, epilepsy, Alzheimer's, and Huntington's. miRNAs regulate cell-signaling regulatory networks at the post-transcriptional level, resulting in controlled cellular development responsive to extracellular stimuli. miRNAs also control the expression of genetic outputs during neuronal development. This neuronal cellular process is tightly regulated and tuned by acute and/or chronic inflammatory cues that, when disrupted, result in the onset of various neurological disorders. This review highlights miRNAs that modulate the neuroinflammatory state within the central nervous system and elucidates the underlying mechanisms that promote or abrogate excessive inflammatory signaling as these biomolecules may become new therapeutic targets in the treatment of chronic neurological disorders such as epilepsy, ALS, Parkinson's, Alzheimer's, and Huntington's. miRNAs are small ncRNAs that modulate gene expression by binding to complementary sequences predominantly within the 3'UTR of target mRNAs. miRNAs are endogenously expressed in the genome and transcribed in the nucleus by RNA polymerase II/III. The resulting primary miRNA (pri-miRNA) transcript is unique in that the pri-miRNA folds creating hairpin bulges similar to tRNA, which is recognized by the RNaseIII enzyme DROSHA. Pri-miRNAs can originate from large intergenic regions of the genome, as well as from intronic regions, and sometimes are polycistronic and contain multiple mature miRNA sequences. The biogenesis of miRNAs involves a series of enzymatic cleavages and processing steps, resulting in the production of mature miRNA duplexes that can be incorporated into RISC complexes to regulate gene expression. miRNAs play a significant role in the activation or suppression of neuroinflammation by controlling the abundance of central mediators of NLRP3 priming and/or activation of the inflammasome. miR-155, for example, regulates the activity of NF-κB, a major protein complex that controls DNA transcription and cytokine production, supports maturation of dendritic cells, promotes recruitment of neutrophils, stimulates M1 polarization of macrophage and microglial cells