Biochemical and Neuroimmunological Changes Associated with Motor Function Recovery in an Experimental Animal Model of Spinal Cord Injury

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Introduction: Spinal cord injury (SCI) triggers secondary neuroinflammatory and autoimmune cascades inducing autoantibody production against neural antigens, contributing to progressive neurological impairment.This study evaluated the dynamics of motor function and neurotropic autoantibody profiles following experimental SCI using the ELI-Neuro-Test.Material and methods: Experimental spinal injury was induced in 98 adult male outbred rats using a standardized weight-drop model.Voluntary locomotor activity, hindlimb grip strength, and motor coordination were assessed on days 3, 7, and 14 post-injury.Serum IgG autoantibodies against 12 targets were measured using the ELI-Neuro-Test and analyzed via Spearman's correlation.Results: SCI rats demonstrated pronounced, persistent motor deficits through day 14.Neurotropic autoantibody levels progressively increased, with the most pronounced rises in anti-opioid receptor IgG (2.4-fold, p<0.05), anti-NF200 IgG (by 50%, p<0.05), and anti-dopamine receptor IgG (by 45%, p<0.01).Spearman's analysis showed the strongest positive correlations with injury severity for anti-GABA receptor IgG (r=0.962;p<0.001) and anti-β-endorphin IgG (r=0.851;p<0.001).Significant positive correlations were also found for anti-dopamine receptor IgG (r=0.685;p<0.001) and anti-S100B IgG (r=0.623;p<0.001).Conclusion: Experimental SCI induces persistent motor deficits and progressive, marker-specific alterations in neurotropic autoantibody profiles involving structural proteins and neurotransmitter systems.These significant correlations indicate the potential value of the ELI-Neuro-Test panel as a multimarker approach for assessing neuroimmune alterations and experimental SCI severity.