ArticleJournal of orthopaedic translation2026
Causal neurodevelopmental origins of scoliosis: Multi-omics Mendelian randomization reveals brain-region-specific pathways and protein mediators.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Advancing the continuum of orthopaedic translation: Mechanistic insight, regenerative innovation, and converging technologies.Journal of orthopaedic translation · 2026Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The causal relationship between early-life central nervous system (CNS) infections and adolescent idiopathic scoliosis (AIS) remains unresolved, with limited evidence on mediating mechanisms linking neuroanatomical changes to spinal deformity. Method: Through three longitudinal cohorts (n = 57875) and two-step Mendelian randomization (MR) integrating neuroimaging genomics (UK Biobank) and proteomics, we dissected causal pathways from childhood viral encephalitis (VE) to scoliosis. We employed inverse-variance weighted (IVW), MR-Egger regression, and sensitivity analyses (MR-PRESSO) to control for pleiotropy and reverse causation. Results: Childhood VE was associated with a 3.6-fold increased risk of scoliosis (HR = 3.604, 95 % CI: 3.121-4.163, P = 0.001), with lesions in the corpus callosum and cerebellum showing the strongest effects. MR analysis identified seven imaging-derived phenotypes (IDPs) causally linked to scoliosis, including grey matter volume in the left thalamus (OR = 1.451) and isotropic free water fraction in the cerebellar peduncle (OR = 2.408). Mediation MR revealed that brain protein ERBB4 and cerebrospinal fluid protein LBP mediated 34.9 % of the total effect (β = -0.181), highlighting their role in bridging neuroinflammation to spinal deformity. Conclusion: This study offers suggestive evidence for a causal pathway from childhood CNS infections to scoliosis, mediated by specific brain-region damage and protein biomarkers. The translational potential of this article: Clinically, the results support the implementation of scoliosis screening programs in children recovering from CNS infections.
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