Dendritic arbor complexity and spine density changes after repetitive mild traumatic brain injury and neuroprotective treatments.
Dendritic arbor complexity and spine density changes after repetitive mild traumatic brain injury and neuroprotective treatments.
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DOI：
10.1016/j.brainres.2020.147019
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发表时间：
2020-11-01
期刊：
影响因子：
2.9
通讯作者：
Citron BA
中科院分区：
文献类型：
--
作者：
Ratliff WA;Delic V;Pick CG;Citron BA
创伤性脑损伤被描述为最近军事冲突的标志性痛苦，反复脑损伤，特别是与军事和体育活动有关的重复性脑损伤，通常会导致更严重的临床后果。大多数脑外伤都是轻微的，但它们会导致长期的认知障碍，目前还没有有效的治疗方法。在脑损伤患者中观察到的最显著的缺陷之一是记忆丧失，这表明脑损伤可以引起海马区的病理变化。叔丁基对苯二酚和吡格列酮分别激活NRF2和PPAR-γ转录因子，在模型系统中都被证明具有神经保护作用。我们研究了反复轻度脑损伤和同时使用两种因素治疗后海马区的形态变化。我们使用了一种闭合性头部损伤的小鼠模型，在5周内有5次损伤。结果显示，海马齿状回神经元的树突和树突棘之间有明显的形态变化。我们观察到树突的总长度以及树突棘的数量和密度都减少了。我们的治疗部分改善了这些效应，表明NRF2和PPAR-γ转录因子可能是未来治疗人类脑损伤的药物开发的重要靶点。
Traumatic brain injury has been described as the signature affliction of recent military conflicts and repetitive TBIs, particularly associated with military and athletic activities, typically result in more severe clinical effects. The majority of TBIs are mild, but they can result in long term cognitive deficits for which there is no effective treatment. One of the most significant deficits observed in TBI patients is memory loss, which suggests that TBI can induce pathological changes within the hippocampus. tert-butylhydroquinone (tBHQ) and pioglitazone activate the Nrf2 and PPAR-γ transcription factors, respectively, and both have been shown to be neuroprotective in model systems. We examined the morphological changes within the hippocampus following repetitive mild TBI and simultaneous treatment with both factors. We utilized a closed head injury mouse model with five injuries over 5 weeks. Our results showed marked morphological changes among the dendrites and dendritic spines of the neurons of the dentate gyrus of the hippocampus. We observed decreases in overall dendritic length, as well as in the quantity and density of dendritic spines. Our treatment partially ameliorated these effects, suggesting that the Nrf2 and PPAR-γ transcription factors may be important targets for future drug development in the treatment of TBI in humans.
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