Siedhoff Heather R, Chen Shanyan, Song Hailong, Cui Jiankun, Cernak Ibolja, Cifu David X, DePalma Ralph G, Gu Zezong
Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, Columbia, MO, United States.
Harry S. Truman Memorial Veterans' Hospital Research Service, Columbia, MO, United States.
Front Neurol. 2022 Jan 13;12:818169. doi: 10.3389/fneur.2021.818169. eCollection 2021.
Most traumatic brain injuries (TBIs) during military deployment or training are clinically "mild" and frequently caused by non-impact blast exposures. Experimental models were developed to reproduce the biological consequences of high-intensity blasts causing moderate to severe brain injuries. However, the pathophysiological mechanisms of low-intensity blast (LIB)-induced neurological deficits have been understudied. This review provides perspectives on primary blast-induced mild TBI models and discusses translational aspects of LIB exposures as defined by standardized physical parameters including overpressure, impulse, and shock wave velocity. Our mouse LIB-exposure model, which reproduces deployment-related scenarios of open-field blast (OFB), caused neurobehavioral changes, including reduced exploratory activities, elevated anxiety-like levels, impaired nesting behavior, and compromised spatial reference learning and memory. These functional impairments associate with subcellular and ultrastructural neuropathological changes, such as myelinated axonal damage, synaptic alterations, and mitochondrial abnormalities occurring in the absence of gross- or cellular damage. Biochemically, we observed dysfunctional mitochondrial pathways that led to elevated oxidative stress, impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated cell respiration-relevant enzyme activity. LIB also induced increased levels of total tau, phosphorylated tau, and amyloid β peptide, suggesting initiation of signaling cascades leading to neurodegeneration. We also compare translational aspects of OFB findings to alternative blast injury models. By scoping relevant recent research findings, we provide recommendations for future preclinical studies to better reflect military-operational and clinical realities. Overall, better alignment of preclinical models with clinical observations and experience related to military injuries will facilitate development of more precise diagnosis, clinical evaluation, treatment, and rehabilitation.
大多数在军事部署或训练期间发生的创伤性脑损伤(TBI)在临床上为“轻度”,且常由非撞击性爆炸暴露所致。已开发出实验模型来重现导致中度至重度脑损伤的高强度爆炸的生物学后果。然而,低强度爆炸(LIB)所致神经功能缺损的病理生理机制尚未得到充分研究。本综述提供了关于原发性爆炸所致轻度TBI模型的观点,并讨论了由超压、冲量和冲击波速度等标准化物理参数定义的LIB暴露的转化方面。我们的小鼠LIB暴露模型重现了与野外爆炸(OFB)相关的部署场景,导致了神经行为变化,包括探索活动减少、焦虑样水平升高、筑巢行为受损以及空间参考学习和记忆受损。这些功能障碍与亚细胞和超微结构神经病理变化相关,如在无大体或细胞损伤情况下发生的有髓轴突损伤、突触改变和线粒体异常。在生物化学方面,我们观察到线粒体途径功能失调,导致氧化应激升高、裂变-融合动力学受损、线粒体自噬减少、氧化磷酸化降低以及与细胞呼吸相关的酶活性代偿性增加。LIB还诱导总tau、磷酸化tau和淀粉样β肽水平升高,提示导致神经退行性变的信号级联反应启动。我们还将OFB研究结果的转化方面与其他爆炸伤模型进行了比较。通过梳理近期相关研究结果,我们为未来的临床前研究提供建议,以更好地反映军事行动和临床实际情况。总体而言,使临床前模型与军事损伤相关的临床观察和经验更好地契合,将有助于更精确的诊断、临床评估、治疗和康复的发展。