Recently, microRNAs (miRNAs) are reported to be crucial modulators in the pathogenesis and potential treatment of epilepsies. To date, several miRNAs have been demonstrated to be significantly expressed in the epileptic tissues and strongly associated with the development of epilepsy. Specifically, miRNAs regulate synaptic strength, inflammation, neuronal and glial function, ion channels, and apoptosis. Furthermore, peripheral blood miRNAs can also be utilized as diagnostic biomarkers to assess disease risk and treatment responses. Here, we will summarize the recent available literature regarding the role of miRNAs in the pathogenesis and treatment of epilepsy. Moreover, we will provide brief insight into the potential of miRNA as diagnostic biomarkers for early diagnosis and prognosis of epilepsy.

Recently, microRNAs (miRNAs) are emerging as new regulators in the pathogenesis of temporal lobe epilepsy (TLE) and playing a major role in the inflammatory and immune processes. The aim of the present study was to evaluate the dynamic expression of brain-specific miR-183 and miR-135a, brain-enriched miR-125b and miR-128 and inflammation-related miR-30c and miR-27a. Status epilepticus evoked by pilocarpine administeration was used to induce epilepsy in rats. Quantitative polymerase chain reaction was performed on rat hippocampus 2 hours, 3 weeks and 2 months following pilocarpine-induced status epilepticus, representing the acute, latent, and chronic phases, respectively. Expression levels were also measured in hippocampus obtained from TLE patients and normal controls. In the rat model, miR-183, miR-135a and miR-125b were detected upregulated during the acute and chronic phases compared to controls, but not during the latent phase. miR-30c and miR-27a were upregulated in the acute and chronic phases of TLE, while in the latent phase miR-30c was downregulated and miR-27a was upregulated. On the other hand, miR-128 showed significantly downregulated in all phases of TLE development. In TLE patients, miR-183, miR- 135a, miR-125b, miR-30c and miR-27a were upregulated, whereas miR-128 was downregulated. Our study revealed upregulation of miR-183, miR-135a and miR-125b in the seizure-related phases and TLE patients, suggesting that all may provide a potential therapeutic approach for the treatment of TLE, whereas the dysregulation of miR-128, miR-30c and miR-27a may suggest different functions during the process of TLE development.

Accumulating evidence is emerging that microRNAs (miRNAs) are key regulators in controlling neuroinflammatory responses that are known to play a potential role in the pathogenesis of temporal lobe epilepsy (TLE). The aim of the present study was to investigate the dynamic expression pattern of interleukin (IL)-10 as an anti-inflammatory cytokine and miR-187 as a post-transcriptional inflammation-related miRNA in the hippocampus of a rat model of status epilepticus (SE) and patients with TLE. We performed a real-time quantitative PCR and western blot on rat hippocampus 2 h, 7 days, 21 days and 60 days following pilocarpine-induced SE, and on hippocampus obtained from TLE patients and normal controls. To detect the relationship between IL-10 and miR-187 on neurons, lipopolysaccharide (LPS) and IL-10-stimulated neurons were performed. Furthermore, we identified the effect of antagonizing miR-187 by its antagomir on IL-10 secretion. Here, we reported that IL-10 secretion and miR-187 expression levels are inversely correlated after SE. In patients with TLE, the expression of IL-10 was also significantly upregulated, whereas miR-187 expression was significantly downregulated. Moreover, miR-187 expression was significantly reduced following IL-10 stimulation in an IL-10–dependent manner. On the other hand, antagonizing miR-187 promoted the production of IL-10 in hippocampal tissues of rat model of SE. Our findings demonstrate a critical role of miR-187 in the physiological regulation of IL-10 anti-inflammatory responses and elucidate the role of neuroinflammation in the pathogenesis of TLE. Therefore, modulation of the IL-10 / miR-187 axis may be a new therapeutic approach for TLE.

These findings elucidate the potential role of miR-139-5p in NMDA-receptor involvement in TLE development and may provide novel therapeutic targets for the future treatment of TLE.

Glutamate-mediated excitotoxicity is the major neuropathological process contributing to numerous neurological diseases. Recently, emerging evidence indicates that microRNAs (miRNAs) play essential roles in the pathophysiology of a wide range of neurological diseases. Notably, there have been significant developments in understanding the biogenesis of miRNAs, their regulatory mechanisms, and their potential as effective biomarkers and therapies. In the present review, we summarize the recent literature that highlights the versatile roles played by miRNAs in glutamate receptor (GluR)-dependent neurological diseases. Based on the reported studies to date, modulation of miRNAs could emerge as a promising therapeutic target for a variety of neurological diseases that were discussed in this review.