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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Neuronal expression of glutamine synthetase in Alzheimer's disease indicates a profound impairment of metabolic interactions with astrocytes.
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Neuronal expression of glutamine synthetase in Alzheimer's disease indicates a profound impairment of metabolic interactions with astrocytes.

机译：谷氨酰胺合成酶在阿尔茨海默氏病中的神经元表达表明与星形胶质细胞的代谢相互作用严重受损。

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A considerable body of evidence indicates that the activity of glutamine synthetase is decreased in the cerebral cortices of brains affected by Alzheimer's disease. It is difficult to discern the reason for this decrease because it is not known whether the cellular distribution of glutamine synthetase is altered in Alzheimer's disease. Therefore the present study has used immunocytochemistry to compare the cellular distributions of glutamine synthetase in the inferior temporal cortices of six Alzheimer's diseased brains and six age-matched, non-demented brains. Double-label immunocytochemistry has been used to examine whether the distribution of cellular glutamine synthetase is influenced by the distribution of senile plaques. It was found that glutamine synthetase expression in astrocytes is diminished in Alzheimer's disease, particularly in the vicinity of senile plaques. The most striking finding of the present study was that glutamine synthetase was expressed in a subpopulation of pyramidal neurons in all six Alzheimer's diseased brains, whereas glutamine synthetase was not observed in any neurons from control brains. The changed expression of glutamine synthetase may be triggered by toxic agents in senile plaques, a reduced noradrenergic supply to the cerebral cortex, and increased brain ammonia levels. That such dramatic changes occur in the distribution of this critical, and normally stable enzyme, suggests that the glutamate-glutamine cycle is profoundly impaired in Alzheimer's disease. This is significant because impairments of the glutamate-glutamine cycle are known to cause alterations of mood and behaviour, disturbance of sleeping patterns, amnesia, confusion and reduced awareness. Since these behavioural changes are also seen in Alzheimer's disease, it is speculated that they might be attributable to the reduced expression of glutamine synthetase or to impairments of the glutamate-glutamine cycle.
机译：大量证据表明，受阿尔茨海默氏病影响的大脑的大脑皮层中谷氨酰胺合成酶的活性降低。由于尚不清楚在阿尔茨海默氏病中是否改变了谷氨酰胺合成酶的细胞分布，因此很难辨别这种下降的原因。因此，本研究使用免疫细胞化学来比较谷氨酰胺合成酶在六个阿尔茨海默氏病患脑和六个年龄匹配的非痴呆脑的颞下皮质中的细胞分布。双标记免疫细胞化学已用于检查细胞谷氨酰胺合成酶的分布是否受老年斑分布的影响。已发现在阿尔茨海默氏病中，尤其是在老年斑附近，星形胶质细胞中谷氨酰胺合成酶的表达降低。本研究最惊人的发现是谷氨酰胺合成酶在所有六个患阿尔茨海默氏病的大脑锥体神经元的亚群中表达，而在对照大脑的任何神经元中均未观察到谷氨酰胺合成酶。谷氨酰胺合成酶表达的改变可能是由老年斑中的有毒物质，减少了对大脑皮质的去甲肾上腺素能供应以及脑氨水平升高所触发的。在这种关键且通常稳定的酶的分布中发生了如此剧烈的变化，表明谷氨酸-谷氨酰胺循环在阿尔茨海默氏病中受到严重损害。这是重要的，因为已知谷氨酸-谷氨酰胺循环的损伤会引起情绪和行为的改变，睡眠方式的紊乱，健忘症，混乱和意识降低。由于在阿尔茨海默氏病中也观察到了这些行为变化，因此推测它们可能归因于谷氨酰胺合成酶表达降低或谷氨酸-谷氨酰胺循环受损。

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