Yu Fang, Huang Tingting, Ran Yuanyuan, Li Da, Ye Lin, Tian Guiqin, Xi Jianing, Liu Zongjian
Department of Neurology, University of Pittsburgh, Pittsburgh, PA, United States.
Department of Anesthesiology, Westchester Medical Center, New York Medical College, Valhalla, NY, United States.
Front Cell Neurosci. 2021 Aug 5;15:727899. doi: 10.3389/fncel.2021.727899. eCollection 2021.
Stroke remains the leading cause of long-term disability worldwide with significant long-term sequelae. However, there is no highly effective treatment to enhance post-stroke recovery despite extensive efforts in exploring rehabilitative therapies. Neurorehabilitation is recognized as the cornerstone of functional restoration therapy in stroke, where treatments are focused on neuroplastic regulation to reverse neural structural disruption and improve neurofunctional networks. Post-stroke neuroplasticity changes begin within hours of symptom onset and reaches a plateau by 3 to 4 weeks within the global brain in animal studies. It plays a determining role in spontaneous stroke recovery. Microglia are immediately activated following cerebral ischemia, which has been found both proximal to the primary ischemic injury and at the remote brain regions which have functional connections to the primary injury area. Microglia exhibit different activation profiles based on the microenvironment and adaptively switch their phenotypes in a spatiotemporal manner in response to brain injuries. Microglial activation coincides with neuroplasticity after stroke, which provides the fundamental base for the microglia-mediated inflammatory responses involved in the entire neural network rewiring and brain repair. Microglial activation exerts important effects on spontaneous recovery after stroke, including structural and functional reestablishment of neurovascular networks, neurogenesis, axonal remodeling, and blood vessel regeneration. In this review, we focus on the crosstalk between microglial activation and endogenous neuroplasticity, with a special focus on the plastic alterations in the whole brain network and their implications for structural and functional restoration after stroke. We then summarize recent advances in the impacts of microglial phenotype polarization on brain plasticity, trying to discuss the potential efficacy of microglia-based extrinsic restorative interventions in promoting post-stroke recovery.
中风仍然是全球长期残疾的主要原因,会导致严重的长期后遗症。然而,尽管在探索康复治疗方面付出了巨大努力,但目前尚无高效的治疗方法来促进中风后的恢复。神经康复被认为是中风功能恢复治疗的基石,其治疗重点在于神经可塑性调节,以逆转神经结构破坏并改善神经功能网络。在动物研究中,中风后神经可塑性变化在症状发作数小时内开始,并在3至4周内达到全脑平台期。它在中风后的自发恢复中起决定性作用。脑缺血后小胶质细胞会立即被激活,在原发性缺血损伤近端以及与原发性损伤区域有功能连接的远隔脑区均有发现。小胶质细胞根据微环境表现出不同的激活模式,并在时空上自适应地切换其表型以应对脑损伤。小胶质细胞激活与中风后的神经可塑性同时发生,这为小胶质细胞介导的参与整个神经网络重塑和脑修复的炎症反应提供了基础。小胶质细胞激活对中风后的自发恢复具有重要影响,包括神经血管网络的结构和功能重建、神经发生、轴突重塑和血管再生。在本综述中,我们重点关注小胶质细胞激活与内源性神经可塑性之间的相互作用,特别关注全脑网络中的可塑性变化及其对中风后结构和功能恢复的影响。然后我们总结了小胶质细胞表型极化对脑可塑性影响的最新进展,试图探讨基于小胶质细胞的外在恢复性干预措施在促进中风后恢复方面的潜在疗效。