Dubois B, Hauw J J, Ruberg M, Serdaru M, Javoy-Agid F, Agid Y
Rev Neurol (Paris). 1985;141(3):184-93.
Intellectual deterioration may be observed in the course of Parkinson's disease. Since it had been reported that central cholinergic systems degenerate in senile dementia and Alzheimer's disease, we measured the activity of choline acetyltransferase (C.A.T.) and the number of muscarinic receptors in various cortical regions of 12 control subjects and 20 patients and compared these biochemical results with clinical and neuropathological data concerning the patients. Thirteen of the parkinsonian patients showed signs of intellectual decline (moderate in 8, severe in 5) and neuropathological examination of the cortex revealed in 10 cases large number of Alzheimer type senile changes extending beyond the hippocampus. C.A.T. activity was decreased in the cerebral cortex in every patient. The decrease was greater in intellectually deteriorated patients and in the group with numerous senile changes in the cortex. The number of muscarinic receptors was increased in patients that had been treated with anticholinergic drugs until they died, but also in those who had not received these drugs, suggesting and underlying denervation hypersensitivity. In the caudate nucleus, however, neither C.A.T. activity nor muscarinic receptor number was altered, indicating that the cortical cholinergic lesion was specific. Although in most cases dementia in Parkinson's disease was of the Alzheimer type, the case of a demented parkinsonian patient in whom cortical C.A.T. activity was severely decreased, in spite of the absence of cortical histopathological evidence characteristic of Alzheimer's disease, suggests that a parkinsonian dementia different from the Alzheimer type also exists. In Parkinson's disease as in Alzheimer's disease the decrease in C.A.T. activity in the cerebral cortex results from degeneration of the cholinergic neurones in the nucleus of Meynert which projects to the cortex. Although the severity of intellectual deterioration seems in relationship with the extent of degeneration, this could already begin before intellectual impairment is apparent.
帕金森病病程中可能会出现智力衰退。由于已有报道称中枢胆碱能系统在老年痴呆症和阿尔茨海默病中会发生退化,我们测量了12名对照者和20名患者不同皮质区域的胆碱乙酰转移酶(C.A.T.)活性及毒蕈碱受体数量,并将这些生化结果与患者的临床和神经病理学数据进行了比较。13名帕金森病患者出现了智力衰退迹象(8例为中度,5例为重度),对皮质进行神经病理学检查发现,10例患者有大量超出海马体范围的阿尔茨海默型老年改变。每位患者大脑皮质中的C.A.T.活性均降低。在智力衰退患者以及皮质有大量老年改变的组中,这种降低更为明显。接受抗胆碱能药物治疗直至死亡的患者,以及未接受这些药物治疗的患者,其毒蕈碱受体数量均增加,提示存在潜在的去神经超敏反应。然而,尾状核中的C.A.T.活性和毒蕈碱受体数量均未改变,表明皮质胆碱能损伤具有特异性。尽管在大多数情况下,帕金森病中的痴呆属于阿尔茨海默型,但有一例痴呆的帕金森病患者,其皮质C.A.T.活性严重降低,尽管缺乏阿尔茨海默病特征性的皮质组织病理学证据,这表明还存在一种不同于阿尔茨海默型的帕金森病痴呆。与阿尔茨海默病一样,帕金森病中大脑皮质C.A.T.活性的降低是由于投射到皮质的梅纳特核中胆碱能神经元的退化所致。尽管智力衰退的严重程度似乎与退化程度有关,但在智力损害明显之前就可能已经开始了。