Dual axonal and inflammatory biomarkers in traumatic brain injury: Diagnostic performance of tau protein and IL-12.

Traumatic brain injury (TBI) is a leading cause of death and neurological disability worldwide, yet conventional clinical assessment methods often fail to capture the underlying molecular pathology. This study evaluated the diagnostic value of serum Tau protein and interleukin-12 (IL-12) across the full TBI severity spectrum, mild, moderate, severe, and fatal, alongside healthy and control-dead cohorts (n = 182). Serum samples collected within 24 h were analysed by sandwich ELISA, with nonparametric statistics, Spearman correlation, and receiver operating characteristic (ROC) analysis used for evaluation. Tau Protein demonstrated negligible discriminatory ability across severity groups and controls, indicating limited independent diagnostic utility. In contrast, IL-12 levels were generally elevated with increasing TBI severity, with the most pronounced increases in severe and fatal cases. A significant negative correlation with Glasgow Coma Scale scores was observed (ρ = -0.236, p = 0.025), though the trend was not strictly monotonic across all groups, suggesting IL-12 reflects overall inflammatory burden rather than a linear severity gradient. ROC analysis confirmed IL-12 superiority over Tau Protein, particularly in distinguishing moderate from severe and fatal TBI. Elevated IL-12 in fatal TBI compared to non-traumatic fatalities indicates trauma-specific neuroimmune activation, with potential forensic utility. Combined Tau Protein and IL-12 analysis enhanced diagnostic discrimination beyond either marker alone. These findings support a dual-biomarker framework integrating axonal injury and neuroinflammatory markers for a more comprehensive biochemical assessment of traumatic brain injury.