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首页> 外文期刊>Trends in Neurosciences >Are purines mediators of the anticonvulsanteuroprotective effects of ketogenic diets?
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Are purines mediators of the anticonvulsanteuroprotective effects of ketogenic diets?

机译:嘌呤是否是生酮饮食抗惊厥/神经保护作用的介质?

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摘要

Abnormal neuronal signaling caused by metabolic changes characterizes several neurological disorders, and in some instances metabolic interventions provide therapeutic benefits. Indeed, altering metabolism either by fasting or by maintaining a low-carbohydrate (ketogenic) diet might reduce epileptic seizures and offer neuroprotection in part because the diet increases mitochondrial biogenesis and brain energy levels. Here we focus on a novel hypothesis that a ketogenic diet-induced change in energy metabolism increases levels of ATP and adenosine, purines that are critically involved in neuron-glia interactions, neuromodulation and synaptic plasticity. Enhancing brain bioenergetics (ATP) and increasing levels of adenosine, an endogenous anticonvulsant and neuroprotective molecule, might help with understanding and treating a variety of neurological disorders.
机译:由代谢变化引起的异常神经元信号表征几种神经系统疾病,在某些情况下,代谢干预可提供治疗益处。实际上,通过禁食或维持低碳水化合物饮食(生酮饮食)来改变代谢可能会减少癫痫发作并提供神经保护作用,部分原因是饮食会增加线粒体的生物发生和脑能量水平。在这里,我们集中于一个新的假设,即生酮饮食诱导的能量代谢变化会增加ATP和腺苷,嘌呤的水平,而嘌呤在神经元-神经胶质细胞相互作用,神经调节和突触可塑性中至关重要。增强脑生物能学(ATP)和增加内源性抗惊厥和神经保护分子腺苷的水平可能有助于理解和治疗各种神经系统疾病。

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