Otani Kento, Shichita Takashi
Stroke Renaissance Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan.
Division of Biochemistry, Faculty of Pharmacy and Graduate School of Pharmaceutical Science, Keio University, Tokyo, 105-8512, Japan.
Inflamm Regen. 2020 Dec 8;40(1):28. doi: 10.1186/s41232-020-00137-4.
Therapeutic strategies for regulating neuroinflammation are expected in the development of novel therapeutic agents to prevent the progression of central nervous system (CNS) pathologies. An understanding of the detailed molecular and cellular mechanisms of neuroinflammation in each CNS disease is necessary for the development of therapeutics. Since the brain is a sterile organ, neuroinflammation in Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) is triggered by cerebral cellular damage or the abnormal accumulation of inflammatogenic molecules in CNS tissue through the activation of innate and acquired immunity. Inflammation and CNS pathologies worsen each other through various cellular and molecular mechanisms, such as oxidative stress or the accumulation of inflammatogenic molecules induced in the damaged CNS tissue. In this review, we summarize the recent evidence regarding sterile immune responses in neurodegenerative diseases.
在新型治疗药物的研发中,人们期望找到调节神经炎症的治疗策略,以防止中枢神经系统(CNS)疾病的进展。了解每种中枢神经系统疾病中神经炎症的详细分子和细胞机制对于治疗学的发展至关重要。由于大脑是一个无菌器官,阿尔茨海默病(AD)、帕金森病(PD)和肌萎缩侧索硬化症(ALS)中的神经炎症是由脑细胞损伤或中枢神经系统组织中炎症原性分子通过先天免疫和后天免疫的激活而异常积累所引发的。炎症和中枢神经系统疾病通过各种细胞和分子机制相互恶化,例如氧化应激或受损中枢神经系统组织中诱导的炎症原性分子的积累。在这篇综述中,我们总结了关于神经退行性疾病中无菌免疫反应的最新证据。