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The role of miR-10b-5p/Brain-derived Neurotrophic Factor Axis Deregulation in Poststroke Epileptogenesis

ABSTRACT: Objective: Poststroke epilepsy (PSE) is a common complication following stroke, associated with increased mortality, poorer functional outcomes, greater disability, and heightened dementia risk. Currently, no standardized guidelines exist for the primary prevention of PSE, and prophylactic antiseizure medications (ASMs) are not routinely recommended. Management typically begins with ASM initiation after the first unprovoked seizure. Identifying predictive biomarkers is critical for improving post-stroke care and preventing PSE. Materials&Methods: We retrospectively analyzed 25 patients with PSE, ischemic stroke without epilepsy, and epilepsy. Serum-derived miRNA sequencing was conducted to identify differentially expressed miRNAs across the groups. Selected miRNAs were validated by quantitative PCR (qPCR), and target prediction was performed in silico. Brain-derived neurotrophic factor (BDNF), a key regulator of post-stroke recovery and epileptogenesis, was identified as a primary target of miR-10b-5p. BDNF levels were measured using ELISA and correlated with clinical parameters. Results: miRNA profiling revealed significant differences among the groups, with miR-10b-5p expression markedly reduced in PSE patients compared to those with stroke alone. qPCR validation confirmed miR-10b-5p as a potential biomarker distinguishing PSE from stroke. In PSE patients, BDNF concentration correlated with disease duration and latency to first seizure, whereas no such association was observed in stroke or epilepsy groups. Conclusion: Our findings suggest a novel pathophysiological mechanism involving the miR-10b-5p/BDNF axis in PSE development. miR-10b-5p may serve as a promising biomarker for early identification and targeted follow-up of stroke patients at high risk for developing epilepsy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE295327 | GEO | 2026/04/17

REPOSITORIES: GEO

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Project description:BACKGROUND MicroRNAs (miRNAs) are small non-coding RNAs that recognize sites of complementarity of target messenger RNAs, resulting in transcriptional regulation and translational repression of target genes. In Huntington’s disease (HD), a neurodegenerative disease caused by a trinucleotide repeat expansion, miRNA dyregulation has been reported, which may impact gene expression and modify the progression and severity of HD. METHODS: We performed next-generation miRNA sequence analysis in prefrontal cortex (Brodmann Area 9) from 26 HD, 2 asymptomatic HD, and 36 control brains. Neuropathological information was available for all HD brains, including age at disease onset, CAG-repeat size, Vonsattel grade, and Hadzi-Vonsattel striatal and cortical scores, a continuous measure of the extent of neurodegeneration. Linear models were performed to examine the relationship of miRNA expression to these clinical features, and messenger RNA targets of associated miRNAs were tested for gene ontology term enrichment. RESULTS: We identified 75 miRNAs differentially expressed in HD brain (FDR q-value <0.05). Among the HD brains, nine miRNAs were significantly associated with Vonsattel grade of neuropathological involvement and three of these, miR-10b-5p, miR-10b-3p, and miR-302a-3p, significantly related to the Hadzi-Vonsattel striatal score (a continuous measure of striatal involvement) after adjustment for CAG length. Five miRNAs (miR-10b-5p, miR-196a-5p, miR-196b-5p, miR-10b-3p, and miR-106a-5p) were identified as having a significant relationship to CAG length-adjusted age of onset including miR-10b-5p, the mostly strongly over-expressed miRNA in HD cases. Although prefrontal cortex was the source of tissue profiled in these studies, the relationship of miR-10b-5p expression to striatal involvement in the disease was independent of cortical involvement. Correlation of miRNAs to the clinical features clustered by direction of effect and the gene targets of the observed miRNAs showed association to processes relating to nervous system development and transcriptional regulation. CONCLUSIONS: These results demonstrate that miRNA expression in cortical BA9 provides insight into striatal involvement and support a role for these miRNAs, particularly miR-10b-5p, in HD pathogenicity. The miRNAs identified in our studies of postmortem brain tissue may be detectable in peripheral fluids and thus warrant consideration as accessible biomarkers for disease stage, rate of progression, and other important clinical characteristics of HD. 26 Huntington's disease, 2 asymptomatic HD gene positive and 49 neurologically normal control prefrontal cortex samples

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The role of miR-10b-5p/Brain-derived Neurotrophic Factor Axis Deregulation in Poststroke Epileptogenesis

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