Department of Medical Laboratory, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
CNS Neurosci Ther. 2024 May;30(5):e14744. doi: 10.1111/cns.14744.
Stroke is an acute cerebrovascular disease in which brain tissue is damaged due to sudden obstruction of blood flow to the brain or the rupture of blood vessels in the brain, which can prompt ischemic or hemorrhagic stroke. After stroke onset, ischemia, hypoxia, infiltration of blood components into the brain parenchyma, and lysed cell fragments, among other factors, invariably increase blood-brain barrier (BBB) permeability, the inflammatory response, and brain edema. These changes lead to neuronal cell death and synaptic dysfunction, the latter of which poses a significant challenge to stroke treatment.
Synaptic dysfunction occurs in various ways after stroke and includes the following: damage to neuronal structures, accumulation of pathologic proteins in the cell body, decreased fluidity and release of synaptic vesicles, disruption of mitochondrial transport in synapses, activation of synaptic phagocytosis by microglia/macrophages and astrocytes, and a reduction in synapse formation.
This review summarizes the cellular and molecular mechanisms related to synapses and the protective effects of drugs or compounds and rehabilitation therapy on synapses in stroke according to recent research. Such an exploration will help to elucidate the relationship between stroke and synaptic damage and provide new insights into protecting synapses and restoring neurologic function.
中风是一种急性脑血管疾病，由于大脑血液供应突然中断或脑内血管破裂，导致脑组织受损，可引发缺血性或出血性中风。中风发作后，缺血、缺氧、血液成分渗透到脑实质、裂解细胞碎片等因素，不可避免地会增加血脑屏障（BBB）通透性、炎症反应和脑水肿。这些变化导致神经元细胞死亡和突触功能障碍，后者对中风治疗构成重大挑战。
中风后突触功能障碍发生的方式有多种，包括：神经元结构损伤、细胞体中病理性蛋白堆积、突触小泡流动性和释放减少、突触中线粒体运输中断、小胶质细胞/巨噬细胞和星形胶质细胞激活突触吞噬作用，以及突触形成减少。
本综述根据最新研究，总结了与突触相关的细胞和分子机制，以及药物或化合物及康复治疗对中风后突触的保护作用。这种探索将有助于阐明中风与突触损伤的关系，并为保护突触和恢复神经功能提供新的见解。
