ArticleJournal of Alzheimer's disease : JAD2013
Blast exposure causes early and persistent aberrant phospho- and cleaved-tau expression in a murine model of mild blast-induced traumatic brain injury.
Article in Journal of Alzheimer's disease : JAD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mouse closed head traumatic brain injury replicates the histological tau pathology pattern of human disease: characterization of a novel model and systematic review of the literature.Acta neuropathologica communications · 2021Pooled it
- Non-invasive Vagal Nerve Stimulation as a Potential Treatment for Repetitive Blast Trauma.bioRxiv : the preprint server for biology · 2026Article
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Chronic post-traumatic stress disorder-related behavioral traits develop in female rats exposed to repetitive low-level blast injury and are reversible with (2R,6R)-hydroxynorketamine.Frontiers in neurology · 2026Article
- Pontine pathology mediates common symptoms of blast-induced chronic mild traumatic brain injury.Brain communications · 2026Article
- Sex-dependent blood-brain barrier alterations following repeated mild blast traumatic brain injury at varying inter-injury intervals.Experimental neurology · 2025Article
- Blast Overpressure-Induced Neuroinflammation and Axonal Injury in the Spinal Cord of Ferrets.Brain sciences · 2025Article
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Minocycline partially reverses established PTSD-related behavioral traits in rats exposed to repetitive low-level blast injury.Frontiers in neurology · 2025Article
- A brief exploration of the physical properties of single living cells under dynamic loading conditions.Frontiers in bioengineering and biotechnology · 2025Article
- Neuronal BAG3 attenuates tau hyperphosphorylation, synaptic dysfunction, and cognitive deficits induced by traumatic brain injury via the regulation of autophagy-lysosome pathway.Acta neuropathologica · 2024Article
- Macroscopic changes in aquaporin-4 underlie blast traumatic brain injury-related impairment in glymphatic function.Brain : a journal of neurology · 2024Article
- Modeling Highly Repetitive Low-level Blast Exposure in Mice.Journal of visualized experiments : JoVE · 2024Article
- Association of Blast Exposure in Military Breaching with Intestinal Permeability Blood Biomarkers Associated with Leaky Gut.International journal of molecular sciences · 2024Article
- The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.International journal of molecular sciences · 2024Review
- Recent insights from non-mammalian models of brain injuries: an emerging literature.Frontiers in neurology · 2024Review
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- IL-34 exacerbates pathogenic features of Alzheimer's disease and calvaria osteolysis in triple transgenic (3x-Tg) female mice.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Timing matters: Sex differences in inflammatory and behavioral outcomes following repetitive blast mild traumatic brain injury.Brain, behavior, and immunity · 2023Article
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
40 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors.
Funding
Abstract
Mild traumatic brain injury (mTBI) is considered the 'signature injury' of combat veterans that have served during the wars in Iraq and Afghanistan. This prevalence of mTBI is due in part to the common exposure to high explosive blasts in combat zones. In addition to the threats of blunt impact trauma caused by flying objects and the head itself being propelled against objects, the primary blast overpressure (BOP) generated by high explosives is capable of injuring the brain. Compared to other means of causing TBI, the pathophysiology of mild-to-moderate BOP is less well understood. To study the consequences of BOP exposure in mice, we employed a well-established approach using a compressed gas-driven shock tube that recapitulates battlefield-relevant open-field BOP. We found that 24 hours post-blast a single mild BOP provoked elevation of multiple phospho- and cleaved-tau species in neurons, as well as elevating manganese superoxide-dismutase (MnSOD or SOD2) levels, a cellular response to oxidative stress. In hippocampus, aberrant tau species persisted for at least 30 days post-exposure, while SOD2 levels returned to sham control levels. These findings suggest that elevated phospho- and cleaved-tau species may be among the initiating pathologic processes induced by mild blast exposure. These findings may have important implications for efforts to prevent blast-induced insults to the brain from progressing into long-term neurodegenerative disease processes.
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