缺血性脑卒中神经血管单元损伤与重塑的多模态影像学研究

Ischemic stroke can be attributed to the failure of interactions and communications among neurons, glial cells and vessels (neurovascular unit, NVU). Up till now, an effective and noninvasive imaging system, which aims to visualize and quantify the process of NVU injury and plasticity in ischemia in vivo, has yet not been established. Based on previous studies of our group, this project intends to perform novel techniques (CEST, CMRO2, NODDI, STI, VSI) on MCAO model with 7T MR by comparing with histopathology and MOST study, to detect the spatiotemporal characteristics of NVU injury in ischemia, to investigate the relationship between the changes of critical molecules (Glu, Lac, ROS, TSPO) in the pathogenesis of ischemia and the outcome of ischemic penumbra; to clarify the dynamic process and molecular mechanism of neovascularization and its association with neurological function; to unveil the pattern, radiological characteristics, pathology of secondary damage in gray and white matter of the whole brain as well as the associations with neurological function. The theoretical establishment of a noninvasive and in vivo imaging system would further facilitate the exploration of the pathogenesis of ischemia and provide a novel idea for the diagnosis and treatment of neurovascular injury and plasticity.

缺血性脑卒中可归结于神经元、胶质细胞及血管间（神经血管单元）的相互作用和通讯障碍。目前缺乏合适有效的影像学评估体系从整体上对脑缺血神经血管单元损伤与重塑机制进行活体无创性成像。本项目在前期研究基础上，拟采用7T磁共振新技术（CEST、CMRO2、NODDI、STI、VSI等）对MCAO模型进行功能及分子成像，并与组织病理学和MOST对比研究，解析脑缺血发生发展过程中神经血管单元损害的时空变化特征， 探索脑缺血发病机制中关键分子（Glu、Lac、ROS、TSPO）含量变化与缺血半暗带双向转归的关系，阐明微血管新生的动态过程、分子基础以及与神经功能恢复的关系，明确脑缺血后全脑灰质和白质继发性损害的形式、影像学特征、病理基础以及与神经功能恢复的关系。从理论上建立缺血性脑卒中神经血管单元损伤与重塑的活体无创性成像体系，将进一步深化对脑缺血发病机制的认识，并为神经血管损伤与修复治疗提供新的诊治思路。

缺血性脑卒中可归结于神经元、胶质细胞及血管间的相互作用和通讯障碍。目前缺乏合适有效的影像学评估方法从整体上对脑缺血神经血管单元损伤与重塑机制进行活体无创性成像。本项目采用多模态磁共振成像新技术与组织病理学对比研究，解析了脑缺血发生发展过程中神经血管单元损害的时空变化特征；探索并阐明脑缺血发病关键分子含量变化、侧枝循环建立以及与缺血半暗带双向转归的关系；探索继发性远隔损害及脑重塑的影像学特征以及与临床预后的关系。从理论上建立了缺血性脑卒中神经血管单元损伤与重塑的活体无创性成像体系，这将进一步深化对脑缺血发病机制的认识，并为神经血管损伤与修复治疗提供新的诊治思路。