ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
LncRNA THUMPD3-AS1 Regulates Behavioral and Synaptic Structural Abnormalities in Schizophrenia via miR-485-5p and ARHGAP8.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Peripheral lncRNA-IL1RAP Dysregulation in Schizophrenia: A Multi-Omics Bridge Between Immunity and Diagnosis.Brain and behavior · 2026Article
- Neuronal ARHGAP8 controls synapse structure and AMPA receptor-mediated synaptic transmission.Communications biology · 2026Article
- LncRNA THUMPD3-AS1 Regulates Behavioral and Synaptic Structural Abnormalities in Schizophrenia via miR-485-5p and ARHGAP8.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Schizophrenia (SCZ) is characterized by synaptic structural deficits, yet how dysregulated noncoding RNAs (ncRNAs) drive these abnormalities remains unknown. Through integrative multilayered analysis of SCZ data from whole transcriptome sequencing (blood samples), GWAS risk loci, and expression data using pipeline ceRNAxis, the THUMPD3-AS1/miR-485-5p/ARHGAP8 axis is identified as a key regulator of synaptic function. Functional validation reveals that THUMPD3-AS1 acts as a competitive endogenous RNA, sequestering miR-485-5p and thereby derepressing ARHGAP8. Despite suppressing RhoA activity, ARHGAP8 enhances ROCK2 activation through RhoB/C-mediated compensatory mechanisms. Hyperactivation of ROCK2 through this noncanonical pathway disrupted actin cytoskeletal remodeling patterns, leading to increased immature dendritic spines and synaptic ultrastructural defects, which are pathological features associated with SCZ. In vivo, ventral hippocampal (vHip) overexpression of miR-485-5p or targeted knockdown of THUMPD3-AS1 rescued MK-801-induced SCZ-like phenotypes (anxiety, cognitive deficits, and social memory impairments) and restored synaptic ultrastructure. Crucially, this regulatory axis is cross-species conservation, with bidirectional expression changes validated in patient-derived blood and vHip tissues of mice. The findings reveal a novel ncRNA-driven pathogenic cascade in SCZ, where dysregulated RhoB/C-ROCK2 signaling, distinct from classical RhoA pathways, mediates synaptic destabilization. This presents a therapeutic axis for precision interventions targeting noncanonical actin cytoskeletal remodeling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.