Witcher Kristina G, Eiferman Daniel S, Godbout Jonathan P
Department of Neuroscience, The Ohio State University, 333 West 10th Avenue, Columbus, OH, USA.
Department of Surgery, The Ohio State University, 395 West 12th Avenue, Columbus, OH, USA.
Trends Neurosci. 2015 Oct;38(10):609-620. doi: 10.1016/j.tins.2015.08.002.
Traumatic brain injury (TBI) can lead to secondary neuropsychiatric problems that develop and persist years after injury. Mounting evidence indicates that neuroinflammatory processes progress after the initial head injury and worsen with time. Microglia contribute to this inflammation by maintaining a primed profile long after the acute effects of the injury have dissipated. This may set the stage for glial dysfunction and hyperactivity to challenges including subsequent head injury, stress, or induction of a peripheral immune response. This review discusses the evidence that microglia become primed following TBI and how this corresponds with vulnerability to a 'second hit' and subsequent neuropsychiatric and neurodegenerative complications.
创伤性脑损伤(TBI)可导致继发性神经精神问题,这些问题在损伤后数年出现并持续存在。越来越多的证据表明,神经炎症过程在初始头部损伤后会继续发展,并随着时间的推移而恶化。小胶质细胞在损伤的急性影响消散很久之后仍保持一种致敏状态,从而导致这种炎症。这可能为胶质细胞功能障碍和对包括随后的头部损伤、压力或外周免疫反应诱导在内的挑战的过度反应奠定基础。本综述讨论了小胶质细胞在TBI后会致敏的证据,以及这如何与对“二次打击”的易感性以及随后的神经精神和神经退行性并发症相关联。