期刊
TRENDS IN NEUROSCIENCES
卷 31, 期 6, 页码 273-278出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2008.02.009
关键词
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资金
- Howard Hughes Medical Institute Funding Source: Medline
- NCRR NIH HHS [RR017699, P20 RR017699] Funding Source: Medline
- NINDS NIH HHS [NS61290, R15 NS061290, NS29173, R01 NS029173] Funding Source: Medline
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.
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