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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 >Glutamate-glutamine cycling in Alzheimer's disease.
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Glutamate-glutamine cycling in Alzheimer's disease.

机译：谷氨酸-谷氨酰胺循环在阿尔茨海默氏病中。

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In addition to its definitive pathological characteristics, neuritic plaques and neurofibrillary tangles, Alzheimer's disease (AD) brain exhibits regionally variable neuronal loss and synaptic dysfunction that are likely to underlie the symptomatic memory loss and language abnormalities. A number of mechanisms that could give rise to this localized damage have been proposed, amongst which excitotoxicity figures prominently. This is the process, well attested in experimental systems, whereby brain cells are excited to death by the pathophysiological action of the brain's most-abundant excitatory transmitter, glutamate. Glutamate transmission is mediated by a range of ionotropic and metabotropic receptors which, when activated, can lead to depolarization and increased intracellular Ca2+ ion concentration in the cells on which they are located. The action of glutamate is terminated by its removal from these receptor sites by transport into nearby cells, most commonly perisynaptic astrocytes. There it is converted to physiologically inert glutamine and shuttled back to excitatory nerve terminals. Malfunctions in components of the glutamate-glutamine cycle could result in a self-perpetuating neuronal death cascade mediated by glutamate. The approval by the FDA of an ionotropic glutamate receptor antagonist to treat late-stage AD has led to renewed interest in the contribution of altered glutamatergic neurotransmission to disease pathogenesis. This review encompasses those aspects of glutamate-glutamine cycling that are altered in AD.
机译：除其确定的病理特征，神经炎斑块和神经原纤维缠结外，阿尔茨海默氏病（AD）脑还表现出区域可变的神经元丢失和突触功能障碍，这可能是症状性记忆丧失和语言异常的基础。已经提出了许多可能引起这种局部损伤的机制，其中兴奋性毒性显着。这是在实验系统中得到充分证明的过程，大脑中最丰富的兴奋性递质谷氨酸的病理生理作用使脑细胞兴奋到死亡。谷氨酸盐的传递是由一系列离子和代谢亲和性受体介导的，这些受体在被激活后会导致去极化和细胞所处细胞内Ca2 +离子浓度的增加。谷氨酸的作用通过转运到附近的细胞，最常见的是突触周围星形胶质细胞，而从这些受体部位去除而终止。在那里，它转化为生理惰性的谷氨酰胺，然后穿梭回到兴奋性神经末梢。谷氨酸-谷氨酰胺循环的组成部分功能异常可能会导致由谷氨酸介导的自我永存的神经元死亡级联反应。 FDA批准使用离子型谷氨酸受体拮抗剂治疗晚期AD引起了人们对改变谷氨酸能神经传递对疾病发病机制的贡献的新兴趣。这篇综述涵盖了在AD中改变的谷氨酸-谷氨酰胺循环的那些方面。

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