Postoperative cognitive dysfunction (POCD) has been hypothesized to be mediated by surgery-induced neuroinflammation, which is also a key element in the pathobiology of neurodegenerative diseases, stroke, and neuropsychiatric disorders. There is extensive communication between the immune system and the central nervous system (CNS). Inflammation resulting from activation of the innate immune system cells in the periphery can impact central nervous system behaviors, such as cognitive performance. Mast cells (MCs), as the"first responders" in the CNS, can initiate, amplify, and prolong other immune and nervous responses upon activation. In addition, MCs and their secreted mediators modulate inflammatory processes in multiple CNS pathologies and can thereby either contribute to neurological damage or confer neuroprotection. Neuroinflammation has been considered to be linked to neurovascular dysfunction in several neurological disorders. This review will provide a brief overview of the bidirectional relationship of MCs-neurovascular unit communication in neuroinflammation and its involvement in POCD, providing a new and unique therapeutic target for the adjuvant treatment of POCD.

译文

假设术后认知功能障碍 (POCD) 是由手术引起的神经炎症介导的,这也是神经退行性疾病,中风和神经精神疾病的病理生物学中的关键因素。免疫系统和中枢神经系统 (CNS) 之间有广泛的交流。外周固有免疫系统细胞激活引起的炎症会影响中枢神经系统的行为,例如认知能力。肥大细胞 (MCs) 作为中枢神经系统中的 “第一反应者”,在激活后可以启动、放大和延长其他免疫和神经反应。MCs及其分泌的介质在多种中枢神经系统疾病中调节炎症过程,因此可以导致神经损伤或赋予神经保护。神经炎症已被认为与几种神经系统疾病中的神经血管功能障碍有关。这篇综述将简要概述神经炎症中MCs-神经血管单元通信的双向关系及其参与POCD,为POCD的辅助治疗提供了新的独特的治疗靶点。

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