Jendroska K, Lees A J, Poewe W, Daniel S E
Department of Neurology, Charité, Berlin, Germany.
Mov Disord. 1996 Nov;11(6):647-53. doi: 10.1002/mds.870110609.
It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to "early" Alzheimer-type pathology. To determine whether amyloid beta-peptide (A beta) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for A beta. Twenty-three cases with PD had dementia, including all nine with A beta distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable A beta accumulation were not demented. Neither AD nor A beta deposition was increased in PD, furthermore, there was no statistical correlation between the amount of A beta and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to A beta, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or "early" Alzheimer-type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.
帕金森病(PD)患者痴呆发病率的增加是由于阿尔茨海默病(AD)发病率较高还是由于“早期”阿尔茨海默型病理改变尚不清楚。为了确定AD的淀粉样β肽(Aβ)在PD患者大脑中是否更频繁出现,我们使用Aβ组织印迹法检查了50例患者和79例对照。23例PD患者患有痴呆,其中包括所有9例Aβ分布于整个大脑皮层的患者;这些病例中有3例患有AD。相比之下,17例具有类似Aβ积聚的对照中有5例未患痴呆。PD患者中AD和Aβ沉积均未增加,此外,大脑皮层中Aβ的量与路易小体的数量之间无统计学相关性。在14例痴呆与Aβ无关的PD患者中,存在脑血管疾病(4例)、大量皮层路易小体(3例)或脑积水(2例);在另外5例中,痴呆无法用组织病理学改变很好地解释。我们的数据发现PD病例中AD或“早期”阿尔茨海默型病理改变均未增加;然而,提示这两种病理改变之间的协同作用导致了痴呆。