Tarakad Arjun, Jankovic Joseph
Parkinson's Disease Center and Movement Disorder Clinic, Department of Neurology, Baylor College of Medicine, 7200 Cambridge, Suite 9A, Houston, TX 77030-4202, USA.
Fac Rev. 2020 Nov 10;9:6. doi: 10.12703/b/9-6. eCollection 2020.
Though primarily a sporadic condition, Parkinson's disease is increasingly recognized to be a multifactorial disease with a strong genetic component. At a cellular level, disruptions of protein trafficking and recycling, particularly by misfolding, accumulation, and aggregation of α-synuclein, mitochondrial dysfunction, oxidative stress, and other etiopathogenic mechanisms, have been found to result in the death of vulnerable neuronal populations and appear to drive the neurodegeneration underlying Parkinson's disease. The improved understanding of these mechanisms has led to the development of novel pathogenesis-targeted and potentially disease-modifying therapeutic approaches in Parkinson's disease. Until these treatments are fully developed and approved, clinicians must rely on therapies designed to improve quality of life of patients by treating various motor and non-motor symptoms of the disease.
尽管帕金森病主要是一种散发性疾病，但它越来越被认为是一种具有强大遗传成分的多因素疾病。在细胞水平上，已发现蛋白质运输和再循环的破坏，特别是α-突触核蛋白的错误折叠、积累和聚集、线粒体功能障碍、氧化应激以及其他致病机制，会导致脆弱神经元群体的死亡，并似乎推动了帕金森病潜在的神经退行性变。对这些机制的深入了解已促使在帕金森病中开发新的针对发病机制且可能改变疾病进程的治疗方法。在这些治疗方法完全开发并获批之前，临床医生必须依靠旨在通过治疗该疾病的各种运动和非运动症状来改善患者生活质量的疗法。
