Lang-Rollin I, Rideout H, Stefanis L
Department of Neurology, Columbia University, New York, NY 10032, USA.
Histol Histopathol. 2003 Apr;18(2):509-17. doi: 10.14670/HH-18.509.
Ubiquitinated inclusions and selective neuronal cell death are considered the pathological hallmarks of Parkinson's disease and other neurodegenerative diseases. Recent genetic, pathological and biochemical evidence suggests that dysfunction of ubiquitin-dependent protein degradation by the proteasome might be a contributing, if not initiating factor in the pathogenesis of these diseases. In neuronal cell culture models inhibition of the proteasome leads to cell death and formation of fibrillar ubiquitin and alpha-synuclein-positive inclusions, thus modeling some aspects of Lewy body diseases. The processes of inclusion formation and neuronal cell death share some common mechanisms, but can also be dissociated at a certain level.
泛素化包涵体和选择性神经元细胞死亡被认为是帕金森病和其他神经退行性疾病的病理标志。最近的遗传学、病理学和生物化学证据表明,蛋白酶体介导的泛素依赖性蛋白质降解功能障碍即便不是这些疾病发病机制的起始因素,也可能是一个促成因素。在神经元细胞培养模型中,蛋白酶体的抑制会导致细胞死亡以及纤维状泛素和α-突触核蛋白阳性包涵体的形成,从而模拟路易体病的某些方面。包涵体形成过程和神经元细胞死亡过程有一些共同机制,但在一定程度上也可能相互分离。