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Exosome-associated tau exacerbates brain functional impairments induced by traumatic brain injury in mice
Molecular and Cellular Neuroscience ( IF 3.5 ) Pub Date : 2018-02-03 , DOI: 10.1016/j.mcn.2018.02.002
Bo Wang , Shuangshuang Han

Traumatic brain injury (TBI) has been associated with an increased risk for neurodegenerative diseases, and Tau spread and accumulation might be one of the mechanisms underlying this process. Exosomes were speculated to be a vehicle for spreading Tau in neurodegenerative diseases. The present study sought to investigate the effect of exosome associated Tau after TBI. C57BL/6J mice were subjected to controlled cortical impact injury and the levels of total and phosphorylated Tau in exosomes were measured. Then we isolated exosomes from wildtype and Tau-knockout mice after TBI. These exosomes were either added to primary cultured neurons to evaluate the toxicity, or injected into brains of mice subjected to TBI to evaluate the effect on brain functions. The levels of total and phosphorylated Tau in exosomes after TBI were significantly elevated. TBI derived exosomes displayed toxicity in primary neuron cultures, exacerbated TBI induced LTP (long-term potentiation) impairment and exacerbated motor and cognitive impairments after TBI. The exosome-associated Tau pathology was one of the mechanisms underlying the long-term neurodegenerative effect after TBI.



中文翻译:

与外来体相关的tau加剧了小鼠外伤性脑损伤所致的脑功能损害

外伤性脑损伤(TBI)与神经退行性疾病的风险增加相关,Tau的扩散和积累可能是该过程的潜在机制之一。外泌体被认为是在神经退行性疾病中传播Tau的媒介。本研究试图调查TBI后与外泌体相关的Tau的作用。C57BL / 6J小鼠受到了可控的皮质撞击损伤,并测量了外泌体中总Tau和磷酸化Tau的水平。然后,我们在TBI后从野生型和Tau基因敲除小鼠中分离出外泌体。这些外泌体或者被添加到原代培养的神经元中以评估毒性,或者被注射到接受TBI的小鼠的大脑中以评估对脑功能的影响。TBI后外泌体中总Tau和磷酸化Tau的水平显着升高。TBI衍生的外泌体在原代神经元培养物中显示出毒性,加剧了TBI诱导的LTP(长期增强)损伤,并在TBI后加剧了运动和认知障碍。外泌体相关的Tau病理学是TBI后长期神经退行性作用的基础机制之一。

更新日期:2018-02-03
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