Diversity of pathological features other than Lewy bodies in familial Parkinson's disease due to SNCA mutations.

American journal of neurodegenerative disease Pub Date : 2013-11-29 eCollection Date: 2013-01-01
Hiroshige Fujishiro, Akiko Yamashita Imamura, Wen-Lang Lin, Hirotake Uchikado, Margery H Mark, Lawrence I Golbe, Katerina Markopoulou, Zbigniew K Wszolek, Dennis W Dickson
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Abstract

The clinical features of the genetically determined forms of familial Parkinson's disease (PD) have been described in multiple reports, but there have been few comparative neuropathologic studies. Five familial PD cases, with mutations in SNCA, were matched for age, sex, and Alzheimer type pathology with sporadic PD cases. Immunohistochemistry for phospho-tau and α-synuclein was performed in 8 brain regions. The frequency of tau pathology and the morphologic features of α-synuclein pathology in familial PD were compared with sporadic PD using semi-quantitative methods. In familial PD, there were significantly more tau positive extra-perikaryal spheroid-like and thread-like lesions than in the sporadic PD. There was no significant difference in the amount of α-synuclein positive neuronal perikaryal pathology between familial PD and sporadic PD, but α-synuclein positive oligodendroglial and neuritic lesions were significantly greater in familial PD compared to sporadic PD. In the substantia nigra, familial PD had more marked neuronal loss and fewer residential neurons with Lewy bodies than the sporadic PD, suggesting a close relationship between the severity of neuronal loss and Lewy body formation. The results show a diversity of pathological features of genetically determined familial PD, and they draw attention to the possible role of tau protein in neurodegeneration. Moreover, the presence of oligodendroglial inclusions at the light and electron microscopic levels in familial PD suggests that PD and multiple system atrophy form a continuum of α-synuclein pathology.

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SNCA突变导致家族性帕金森病除路易体外病理特征的多样性
遗传决定的家族性帕金森病(PD)的临床特征已在多个报告中描述,但很少有比较的神经病理学研究。5例SNCA基因突变的家族性PD病例与散发性PD病例的年龄、性别和阿尔茨海默病型病理相匹配。对8个脑区进行磷酸化tau蛋白和α-突触核蛋白的免疫组化。采用半定量方法比较家族性PD与散发性PD的tau病理频率及α-突触核蛋白病理形态学特征。在家族性PD中,tau阳性的核周外球状和线状病变明显多于散发性PD。家族性PD与散发性PD中α-突触核蛋白阳性的神经元核周病变数量无显著差异,但家族性PD中α-突触核蛋白阳性的少突胶质和神经性病变明显多于散发性PD。在黑质中,家族性PD比散发性PD有更明显的神经元丢失和更少的路易体驻留神经元,提示神经元丢失的严重程度与路易体形成密切相关。这些结果显示了遗传决定的家族性PD的多种病理特征,并引起了人们对tau蛋白在神经变性中的可能作用的关注。此外,在光镜和电镜水平上,家族性PD中少突胶质包涵体的存在表明PD和多系统萎缩形成了α-突触核蛋白病理的连续体。
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