Struble R G, Cork L C, Whitehouse P J, Price D L
Science. 1982 Apr 23;216(4544):413-5. doi: 10.1126/science.6803359.
Although several studies of Alzheimer's disease suggest that the frequency of neuritic plaques in the cerebral cortex is correlated with the severity of dementia and with reduction in presynaptic cholinergic markers in the cortex, the relationship between cholinergic cortical innervation and the pathogenesis of plaques is unknown. The hypothesis was tested that the neurites in the plaque consist, in part, of presynaptic cholinergic axons, many of which arise from neurons in the basal forebrain. This hypothesis was tested by analyzing the character and distribution of plaques in monkeys, aged 4 to 31 years, with staining for acetylcholin-esterase and also with Congo red and silver stains. Immature and mature plaques were rich in acetylcholinesterase. As the plaques matured, the amount of amyloid increased, and the number of neurites and the activity of acetylcholinesterase decreased. End-stage amyloid-rich plaques lacked acetylcholinesterase. These observations indicate that changes in cortical cholinergic innervation are an important feature in the pathogenesis and evolution of the neuritic plaque.
尽管多项关于阿尔茨海默病的研究表明，大脑皮质中神经炎性斑块的频率与痴呆的严重程度以及皮质中突触前胆碱能标志物的减少相关，但胆碱能皮质神经支配与斑块发病机制之间的关系尚不清楚。有一个假说接受了检验，即斑块中的神经突部分由突触前胆碱能轴突组成，其中许多轴突起源于基底前脑的神经元。通过对4至31岁猴子的斑块特征和分布进行分析来检验这一假说，采用乙酰胆碱酯酶染色以及刚果红和银染色。未成熟和成熟的斑块富含乙酰胆碱酯酶。随着斑块成熟，淀粉样蛋白量增加，神经突数量和乙酰胆碱酯酶活性降低。晚期富含淀粉样蛋白的斑块缺乏乙酰胆碱酯酶。这些观察结果表明，皮质胆碱能神经支配的变化是神经炎性斑块发病机制和演变的一个重要特征。
