Abstract Repeated low-intensity blast overpressure exposures, frequently sustained by Special Operations Forces during breaching, combat training, and weapons use, are thought to initiate tau-related neurodegenerative changes that may remain clinically silent for years. The long-term impact of cumulative blast overpressure on brain health is poorly understood, and sensitive biomarkers are needed for early detection and monitoring of subclinical injury in high-risk populations. In this cross-sectional study, 25 actively serving male Canadian Special Operations Forces personnel (mean SD age, 43.6 6.1 years) with ≥16 years of breaching and explosives experience were compared with 10 age-matched Canadian Armed Forces controls (mean SD age, 39.8 6.8 years) with minimal blast exposure. All participants underwent 18Fflortaucipir PET imaging to quantify cortical tau deposition, MRI, ultrasensitive digital immunoassay for plasma biomarkers, and comprehensive clinical and neurocognitive testing. Group differences in regional 18Fflortaucipir standardized uptake value ratios were assessed using analysis of covariance, and voxelwise Z-score mapping identified clusters of elevated tracer uptake (2 SD above control mean). Linear regression analyses were conducted to examine associations between PET tau signal, plasma biomarkers, cumulative blast exposure, and clinical outcomes. Special Operations Forces personnel exhibited significantly higher 18Fflortaucipir uptake in the frontal (p = 0.022) and temporal cortices (p = 0.037) compared with controls. Voxelwise mapping revealed tau clusters in 88% of exposed individuals, with nearly half localized to the frontal cortex. Elevated PET signal correlated with cumulative years of breaching, post-concussive symptoms, sleep disturbance, and functional impairment. Plasma biomarkers showed converging evidence of neurodegeneration: brain-derived tau, glial fibrillary acidic protein, and amyloid-β42 levels were significantly associated with regional tau PET uptake. A reduced amyloid-β42/40 ratio and elevated phosphorylated tau isoforms further supported early molecular changes consistent with neurodegeneration. Cumulative occupational blast overpressure exposure in Special Operations Forces is associated with frontal-predominant tau deposition and plasma biomarker signatures of astroglial activation, axonal injury, and CNS-specific tau release. These convergent imaging and molecular findings support a link between repetitive blast exposure and early-stage tauopathy, and highlight the value of combined tau PET imaging and fluid biomarkers as noninvasive tools for early detection, monitoring, and targeted risk mitigation in blast-exposed populations.
Lora et al. (Wed,) studied this question.
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