ArticleBMC neuroscience2026
Whole-transcriptome sequencing reveals Alzheimer's disease-associated ceRNA regulatory networks and downstream pathways.
Article in BMC neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveAlzheimer's disease (AD) molecular mechanisms remain unclear, and effective therapies are lacking. This study employed whole-transcriptome sequencing to investigate the expression profiles of circRNAs, lncRNAs, miRNAs, and mRNAs in the hippocampus of APP/PS1 transgenic mice, aiming to identify ceRNA regulatory networks and clarify their roles in AD pathogenesis.
methodsDifferentially expressed RNAs were integrated into ceRNA networks, and programmed cell death-related pathways were analyzed using GO and KEGG. The computationally predicted circRNA_13083/miR-298-5p/CD14 axis was preliminarily evaluated in vitro using siRNA-mediated CD14 knockdown in microglial and neuronal AD models. Expression of CD14, NF-κB components, and NLRP3 markers was measured by qRT-PCR, while secreted IL-1β and IL-18 protein levels were quantified via ELISA. Neuronal survival was assessed via CCK-8 assays.
resultsTranscriptome analysis revealed 376 differentially expressed mRNAs, 491 lncRNAs, 5,253 circRNAs, and 21 miRNAs, which formed extensive ceRNA interaction networks. Functional enrichment highlighted programmed cell death pathways, including NF-κB and inflammasome signaling. The circRNA_13083/miR-298-5p/CD14 axis emerged as a key regulatory node. qRT-PCR confirmed elevated CD14 expression in AD models. CD14 knockdown significantly attenuated Aβ1-42-induced NF-κB activation, NLRP3 inflammasome assembly, and proinflammatory cytokine release. Conditioned medium transfer experiments further demonstrated that CD14 silencing alleviated microglia-mediated neuronal damage and improved HT-22 cell survival.
conclusionWhole-transcriptome sequencing uncovered extensive ceRNA regulatory networks in AD hippocampus, with the circRNA_13083/miR-298-5p/CD14 axis potentially implicated in neuroinflammation and programmed cell death through NF-κB signaling. Silencing CD14 mitigates microglial activation and neuronal injury, highlighting its potential as a therapeutic target for AD.
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