小胶质细胞
神经炎症
神经保护
帕金森病
神经科学
粒体自噬
自噬
氧化应激
炎症
医学
疾病
人口
免疫学
生物
病理
内科学
细胞凋亡
环境卫生
生物化学
作者
Katja Badanjak,Sonja Fixemer,Semra Smajić,Alexander Skupin,Anne Grünewald
摘要
With the world’s population ageing, the incidence of Parkinson’s disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.
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