Traumatic brain injury (TBI) is the leading cause of morbidity and mortality worldwide. Although TBI leads to mechanical damage during initial impact, secondary damage also occurs as results from delayed neurochemical process and intracellular signaling pathways. Accumulated animal and human studies demonstrated that apoptotic mechanism contributes to overall pathology of TBI. Apoptotic cell death has been identified within contusional brain lesion at acute phase of TBI and in region remote from the site directly injured in days to weeks after trauma. TBI is also dynamic conditions that cause neuronal decline overtime and is likely due to neurodegenerative mechanisms years after trauma. Current studies have even suggested association of neuronal damage through apoptotic pathway with mild TBI, which contributes chronic persistent neurological symptoms and cognitive deficits. Thus, a better understanding of the acute and chronic consequences of apoptosis following TBI is required. The purpose of this review is to describe (1) neuronal apoptotic pathway following TBI, (2) contribution of apoptosis to acute and chronic phase of TBI, and (3) current treatment targeting on apoptotic pathway.

中文翻译：

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外伤性脑损伤中的细胞死亡和恢复。

颅脑外伤（TBI）是全球发病率和死亡率的主要原因。尽管TBI在初始撞击过程中会导致机械损伤，但继发性神经化学过程和细胞内信号通路的延迟也会导致继发损伤。大量的动物和人体研究表明，凋亡机制有助于TBI的整体病理。在创伤后几天至几周内，已在TBI急性期的挫伤性脑病变内以及远离直接受伤部位的区域中发现了凋亡细胞死亡。TBI也是动态状况，会导致神经元随着时间的推移而下降，并且很可能是由于创伤后数年的神经退行性机制所致。目前的研究甚至表明，通过凋亡途径引起的神经元损伤与轻度TBI，造成慢性持续性神经症状和认知缺陷。因此，需要更好地了解TBI后细胞凋亡的急性和慢性后果。这篇综述的目的是描述（1）TBI后的神经元凋亡途径，（2）细胞凋亡对TBI急性期和慢性期的贡献，以及（3）针对凋亡途径的当前治疗方法。