ArticleFrontiers in neurology2025
Modeling biomarker kinetics of Aβ levels in serum following blast.
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Integrated Blood Biomarker and Neurobehavioural Signatures of Latent Neuroinjury in Experienced Military Breachers Exposed to Repetitive Low-Intensity Blast.International journal of molecular sciences · 2026Article
- Tau-PET imaging and blood biomarkers reveal early tauopathy in special operations forces exposed to repetitive blast.Brain communications · 2026Article
- Mechanistic modeling of amyloid dynamics relating to Alzheimer's disease progression.Frontiers in aging neuroscience · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elucidating the unique neuropathological response to blast exposure remains a barrier towards the development of diagnostic approaches for those with blast-induced traumatic brain injury (bTBI). Quantification of biomarker concentrations in the blood post-injury is typically used to inform brain injury severity. However, injury progression and associated changes in biomarker concentrations are sensitive to parameters such as the blast overpressure (BOP) magnitude and frequency of blast exposure. Through this work, a blast-dose biomarker kinetics (BxK) platform was developed and validated for Aβ42 as a promising predictor of injury post-blast. Blast-dose responses accounting for BOP magnitude and frequency were integrated into a mathematical model accounting for whole-body Aβ peptide kinetics. Validation of the developed model was performed through comparison with acute monomer levels in the blood serum of 15 service members exposed to repeated low-level blast while undergoing three-day weapons training. Amyloid precursor protein (APP) synthesis was assumed to be proportional to blast magnitude and additive effects within a window of recovery were applied to account for cumulative exposure. Aβ42 concentrations in the blood serum were predicted within 6.5 ± 5.2% on average, demonstrating model feasibility and biomarker sensitivity to blast. Outcomes discuss how modulation of patient-specific factors (age, weight, genetic factors, years of exposure, sleep) and pathophysiological factors (BBB permeability, amyloidogenic pathology, neuroinflammation) can reveal potential sources of variability in experimental data and be incorporated into the blast-dose BxK platform in future iterations. Advancements in model complexity accounting for sex-specific factors, weapon system, stress levels, risk of symptom onset, and pharmacological treatment strategies are anticipated to improve model calibration. Utilization of this blast-dose BxK model to identify drivers of pathophysiological mechanisms and predict chronic outcomes has the potential to transform bTBI diagnostic, prognostic, and therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.