Mann D M, Yates P O, Hawkes J
Clin Neuropathol. 1983;2(1):1-7.
The number of nerve cells of locus ceruleus and their nucleolar volume were determined in 63 normally aged individuals and in 41 cases with neurologic diseases. Pathologic alterations, such as a severe nerve cell loss and atrophy with or without extensive neurofibrillary degeneration or Lewy body formation, were generally seen in the nucleus locus ceruleus in Alzheimer's disease, Down's syndrome, dementia pugilistica, Parkinson's disease, and progressive supranuclear palsy, but such changes were only slight in normally aged individuals and minimal in motor neuron disease. Protein synthetic capacity was substantially reduced in the remaining nerve cells of the locus ceruleus, in Alzheimer's disease, Down's syndrome, and dementia pugilistica, but was unaltered in normally aged individuals (even in extreme old age), in motor neuron disease, and in the few remaining cells in Parkinson's disease and progressive supranuclear palsy. It is suggested that the pathologic alterations in the locus ceruleus found in these diseases, in conjunction with changes in the hypothalamus, lead to impairment of mental ability with eventual dementia through disturbance of the function of those pathways regulating homeostasis within the central nervous system.
在63名正常老年人和41例患有神经系统疾病的患者中，对蓝斑神经细胞数量及其核仁体积进行了测定。在阿尔茨海默病、唐氏综合征、拳击性痴呆、帕金森病和进行性核上性麻痹中，蓝斑核中通常可见严重的神经细胞丢失和萎缩，伴有或不伴有广泛的神经原纤维变性或路易小体形成等病理改变，但在正常老年人中此类变化轻微，在运动神经元病中则极小。在阿尔茨海默病、唐氏综合征和拳击性痴呆中，蓝斑剩余神经细胞的蛋白质合成能力大幅降低，但在正常老年人（即使是高龄者）、运动神经元病以及帕金森病和进行性核上性麻痹中剩余的少数细胞中，蛋白质合成能力未发生改变。有人提出，这些疾病中蓝斑出现的病理改变，连同下丘脑的变化，通过干扰中枢神经系统内调节内环境稳定的那些通路的功能，导致智力受损，最终发展为痴呆。
