# Tau-PET imaging and blood biomarkers reveal early tauopathy in special operations forces exposed to repetitive blast

**Authors:** Shamantha J Lora, Shawn G Rhind, Sarah E Watling, Lucas Narciso, Jerry Warsh, Oshin Vartanian, Tina McCluskey, Rachel F Tyndale, Maria Carmela Tartaglia, Maria Y Shiu, Isabelle Vallée, Mike Crouzat, Iain Vergie, Neil Vasdev, Isabelle Boileau

PMC · DOI: 10.1093/braincomms/fcag070 · Brain Communications · 2026-03-13

## TL;DR

Special Operations Forces exposed to repeated blasts show early signs of brain damage, detectable through brain scans and blood tests.

## Contribution

Combines PET imaging and blood biomarkers to reveal early tauopathy in blast-exposed military personnel.

## Key findings

- Special Operations Forces showed higher tau deposition in frontal and temporal cortices compared to controls.
- Plasma biomarkers indicated neurodegeneration linked to blast exposure and tau PET findings.
- Biomarker and imaging data suggest early molecular changes consistent with brain injury.

## 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 [18F]flortaucipir PET imaging to quantify cortical tau deposition, MRI, ultrasensitive digital immunoassay for plasma biomarkers, and comprehensive clinical and neurocognitive testing. Group differences in regional [18F]flortaucipir 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 [18F]flortaucipir 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 non-invasive tools for early detection, monitoring, and targeted risk mitigation in blast-exposed populations.

Lora et al. reported that repeated low-intensity blast exposure in Special Operations Forces was linked to increased frontal-predominant tau deposition using PET and elevations in plasma biomarkers of astroglial and neuronal injury. These findings highlight the need for enhanced monitoring, personalized risk evaluation and proactive protection of military brain health.

Graphical Abstract

## Linked entities

- **Proteins:** MAPT (microtubule associated protein tau)

## Full-text entities

- **Genes:** MAOB (monoamine oxidase B) [NCBI Gene 4129], APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, LRP1 (LDL receptor related protein 1) [NCBI Gene 4035] {aka A2MR, APOER, APR, CD91, DDH3, IGFBP-3R}, APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, UCHL1 (ubiquitin C-terminal hydrolase L1) [NCBI Gene 7345] {aka HEL-117, HEL-S-53, NDGOA, PARK5, PGP 9.5, PGP9.5}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, NEFL (neurofilament light chain) [NCBI Gene 4747] {aka CMT1F, CMT2E, CMTDIG, NF-L, NF68, NFL}
- **Diseases:** GAD-7 (MESH:C000726808), neurocognitive deficits (MESH:D009461), amyloid (MESH:C000718787), synaptic dysfunction (MESH:C536122), regulation (MESH:C564833), psychological impairments (MESH:D000067073), neurotoxic (MESH:D020258), cognitive (MESH:D003072), sleep disturbance (MESH:D012893), mood disturbance (MESH:D019964), substance use disorder (MESH:D019966), neuroinflammation (MESH:D000090862), anxiety symptoms (MESH:D001008), Operator Syndrome (MESH:D010149), irritability (MESH:D001523), AD (MESH:D000544), plasma abnormalities (MESH:D007952), headache (MESH:D006261), anxiety (MESH:D001007), mitochondrial dysfunction (MESH:D028361), TBI (MESH:D000070642), BBB dysfunction (MESH:C536830), and neuronal injury (MESH:D009410), Head injuries (MESH:D006259), memory changes (MESH:D008569), neuronal and glial injury (MESH:D016472), neuropathological (MESH:D009422), CTE (MESH:D000070627), attention-deficit/hyperactivity disorder (MESH:D001289), IV (MESH:D006011), loss of consciousness (MESH:D014474), neurodegeneration (MESH:D019636), tinnitus (MESH:D014012), concussion (MESH:D001924), SOF (MESH:D012678), axonal injury (MESH:D001480), Alzheimer tauopathy (MESH:D024801), neuroaxonal injury (MESH:D019150), axonal and (MESH:D012183), injury (MESH:D014947), post (MESH:D000094025), post-concussive symptom (MESH:D038223), dementia (MESH:D003704), CAF (MESH:D001134), NFTs (MESH:D055956), blast (MESH:D001753), brain injury (MESH:D001930), cortical atrophy (MESH:D001284), epilepsy (MESH:D004827), PTSD (MESH:D013313), multiple sclerosis (MESH:D009103), Symptom (MESH:D012816), sleep disruption (MESH:D019958), vascular damage (MESH:D057772), aggression (MESH:D010554), Depression (MESH:D003866), astrogliosis (MESH:D005911)
- **Chemicals:** alcohol (MESH:D000438), [18F]FDDNP (MESH:C444520), polypropylene (MESH:D011126), A-beta1 (-), salt (MESH:D012492), [18F]]flortaucipir (MESH:C000591008)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** rs429358, rs7412

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## References

88 references — full list in the complete paper: https://tomesphere.com/paper/PMC12993815/full.md

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Source: https://tomesphere.com/paper/PMC12993815