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small non-coding RNAs in targeting inflammation in epilepsy.
Conclusion
Taken together, we aimed to characterize TSC tubers on histological, transcriptomic and epigenetic level, in order to find targets for further investigation which ultimately will lead to improved pharmacological treatment and outcome in TSC. Inflammatory pathways are amongst the main deregulated systems in TSC tubers and therefore repre- sent excellent targets for further exploration. With an multi-platform analysis of a large cohort of TSC tubers, we now indicated specific deregulated biological signaling path- ways and potential targets for treatment. One possible target for therapeutic interven- tion is the immunoproteasome, since the expression of specific subunits was increased and correlated with seizure frequency. Additionally, we pinpointed several miRNAs; the miR34 family, miR146a, and miR147b that are deregulated in TSC. Due to their potent neg- ative regulation of inflammatory signaling in vitro, these miRNAs deserve further investi- gation potential therapy in neurological disorders associated with inflammation, such as epilepsy. In the past few years, research into the potential therapeutic value of miRNAs in treating drug-resistant epilepsy is emerging and pre-clinical and clinical studies are encouraging. Therefore, administration of miRNAs could therefore be a promising new therapy in the treatment of epilepsy and TSC.