Mauceli Giuseppe, Busceti Carla I, Pellegrini Antonio, Soldani Paola, Lenzi Paola, Paparelli Antonio, Fornai Francesco
Department of Human Morphology and Applied Biology, University of Pisa, Via Roma, 55, I-56126 Pisa, Italy.
Ann N Y Acad Sci. 2006 Aug;1074:191-7. doi: 10.1196/annals.1369.019.
alpha-Synuclein is a presynaptic protein involved in various degenerative disorders now defined as synucleinopathies. These include neurological diseases that share a few pathological features consisting of aggregates of both normal and altered alpha-synuclein within specific neuronal populations and/or glial cells. The prototype of synucleinopathies is represented by Parkinson's disease (PD) in which alpha-synuclein is identified as a constant component of neuronal pale eosinophilic inclusions: "the Lewy Bodies." In the present article, we discuss the potential significance of amphetamine-induced overexpression of alpha-synuclein in light of clinical findings showing neurodegeneration following overexpression of alpha-synuclein and recent experimental studies that measured increased expression of alpha-synuclein following amphetamine derivatives.
α-突触核蛋白是一种突触前蛋白，参与多种现在被定义为突触核蛋白病的退行性疾病。这些疾病包括一些神经疾病，它们具有一些病理特征，即在特定神经元群体和/或神经胶质细胞内存在正常和改变的α-突触核蛋白聚集体。突触核蛋白病的原型是帕金森病（PD），其中α-突触核蛋白被确定为神经元淡嗜酸性包涵体“路易小体”的恒定成分。在本文中，鉴于临床研究结果显示α-突触核蛋白过表达后会出现神经退行性变，以及最近的实验研究测量了苯丙胺衍生物后α-突触核蛋白表达增加，我们讨论了苯丙胺诱导的α-突触核蛋白过表达的潜在意义。
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