Volume 44 Issue 12
Dec.  2024
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BAO Yunyu, XIN Jiayan, ZHANG Anqiang, WANG Yanjiang, BU Xianle. Research progress on the pathogenesis and biomarkers of blast-induced traumatic brain injury[J]. Explosion And Shock Waves, 2024, 44(12): 121412. doi: 10.11883/bzycj-2024-0179
Citation: BAO Yunyu, XIN Jiayan, ZHANG Anqiang, WANG Yanjiang, BU Xianle. Research progress on the pathogenesis and biomarkers of blast-induced traumatic brain injury[J]. Explosion And Shock Waves, 2024, 44(12): 121412. doi: 10.11883/bzycj-2024-0179

Research progress on the pathogenesis and biomarkers of blast-induced traumatic brain injury

doi: 10.11883/bzycj-2024-0179
  • Received Date: 2024-06-12
  • Rev Recd Date: 2024-10-14
  • Available Online: 2024-10-15
  • Publish Date: 2024-12-01
  • Blast-induced traumatic brain injury (bTBI) is defined as the damaging effect of the shock wave on the brain, which may cause behavioral impairment, physical symptoms and long-term cognitive impairment. Statistically, bTBI is the most common type of traumatic brain injury in combatants, but the mechanism has not been fully elucidated so far because of the high complexity of bTBI. When the shock wave produced during explosions acts on the surface of the skull and propagates within the head, it can lead to a diffuse damage to the brain. In terms of pathological mechanism, bTBI includes two aspects: primary injury and secondary injury. The mechanical injury effect of the shock wave generated by explosions can cause the primary injury of craniocerebral structures, which is usually irreversible and can be only prevented with effective measures. And the secondary injuries will be triggered by the primary injury after bTBI, which involve a series of complex cascades including synaptic dysfunction, excitotoxic injury, blood-brain barrier disruption, meningeal lymphatic system dysfunction, neuroinflammation, mitochondrial dysfunction, oxidative stress, tau protein hyperphosphorylation and amyloid-β pathological changes. And it can last for some time or even extend into the chronic stage after injury, providing a critical window for intervention. It is difficult to diagnose mild bTBI due to the high heterogeneity of clinical symptoms and the positive imaging manifestations. However, great progresses have been made in the research of blood biomarkers of bTBI in recent years, such as ubiquitin carboxyl-terminal hydrolase L1, neuron-specific enolase, neurofilament protein-light, hyperphosphorylated tau protein, myelin basic protein, glial fibrillary acidic protein, S100 calcium-binding protein B and other novel biomarkers. All of the above-mentioned biomarkers are expected to be effective means of early diagnosis and prognosis judgment of imaging-negative bTBI. In conclusion, this review focuses on the frontier progress of the pathogenesis and biomarkers of bTBI, and looks forward to future research directions in order to provide more new ideas for exploring the pathogenesis, early diagnosis strategies as well as intervention targets of bTBI.
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