Understanding how dopaminergic neurons die in Parkinson's disease is crucial to identify which cellular pathways and molecular targets are amenable to therapeutic intervention. Using neurons from patients with Parkinson's disease, Burbulla and colleagues¹ identified a toxic cascade of mitochondrial and lysosomal dysfunction mediated by the accumulation of oxidised dopamine and α-synuclein. However, this pathogenic cascade was not found in mouse models of Parkinson's disease because of species-specific differences in dopamine metabolism that allow the survival of mouse dopaminergic neurons.

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2017年帕金森氏病高度优先出版物

了解多巴胺能神经元如何在帕金森氏病中死亡对于确定哪些细胞途径和分子靶标适合治疗干预至关重要。Burbulla等[ ^1]使用帕金森氏病患者的神经元，发现了由氧化多巴胺和α-突触核蛋白的积累介导的线粒体和溶酶体功能障碍的毒性级联反应。但是，在致帕金森氏病的小鼠模型中未发现这种致病级联，因为多巴胺代谢的物种特异性差异使小鼠多巴胺能神经元得以存活。