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α-突触核蛋白免疫反应性皮质路易小体与帕金森病的认知障碍有关。

Alpha-synuclein-immunoreactive cortical Lewy bodies are associated with cognitive impairment in Parkinson's disease.

作者信息

Mattila P M, Rinne J O, Helenius H, Dickson D W, Röyttä M

机构信息

Department of Pathology, University of Turku, Finland.

出版信息

Acta Neuropathol. 2000 Sep;100(3):285-90. doi: 10.1007/s004019900168.

DOI:10.1007/s004019900168
PMID:10965798
Abstract

Amygdala, hippocampus and six cortical gyri were examined for the Lewy body (LB) degeneration and Alzheimer's disease (AD) type changes in 45 patients with Parkinson's disease (PD). For detection of LBs, the brain areas were stained with an antibody against alpha-synuclein. The extent of neuropathological lesions was investigated in relation to cognitive dysfunction and apolipoprotein E (apoE) epsilon4 allele dosage. At least one cortical LB was found in 95% of cases (43/45). Furthermore, 40% of cases (18/45) had histological findings of definite AD (CERAD class C). Those PD cases with the apoE epsilon4 allele had a significantly greater number of cortical LBs than those without the apoE epsilon4 allele, but this was statistically significant only in precentral, angular and temporal gyri. The LB density correlated better with the number of plaques than with the density of tangles. The number of LBs in several cortical areas correlated significantly with the cognitive impairment. In stepwise linear regression analysis, the number of LBs in the cingulate gyrus and the amount of tangles in the temporal cortex remained statistically significant. When the CERAD class C was excluded, the correlation between cognitive decline and the number of LBs in cortical areas became even more pronounced. A stepwise linear regression analysis in these cases found the number of LBs in the frontal gyrus to be the statistically most significant predictor of cognitive impairment. This study shows, for the first time, that in PD, alpha-synuclein-positive cortical LBs are associated with cognitive impairment independent of AD-type pathology.

摘要

对45例帕金森病(PD)患者的杏仁核、海马和6个脑回进行了路易体(LB)变性及阿尔茨海默病(AD)类型改变的检查。为检测路易体,使用抗α-突触核蛋白抗体对脑区进行染色。研究了神经病理损伤程度与认知功能障碍及载脂蛋白E(apoE)ε4等位基因剂量的关系。95%的病例(43/45)至少发现一个皮质路易体。此外,40%的病例(18/45)有明确的AD组织学表现(CERAD C级)。携带apoE ε4等位基因的PD病例皮质路易体数量显著多于未携带apoE ε4等位基因的病例,但仅在中央前回、角回和颞回具有统计学意义。路易体密度与斑块数量的相关性优于与缠结密度的相关性。几个皮质区域的路易体数量与认知障碍显著相关。在逐步线性回归分析中,扣带回中的路易体数量和颞叶皮质中的缠结数量仍具有统计学意义。排除CERAD C级病例后,皮质区域路易体数量与认知衰退之间的相关性更加明显。对这些病例进行的逐步线性回归分析发现,额回中的路易体数量是认知障碍最具统计学意义的预测指标。这项研究首次表明,在帕金森病中,α-突触核蛋白阳性的皮质路易体与认知障碍相关,且独立于AD型病理。

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