Brain energy metabolism as potential target of neuroprotective strategies

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For a certain number of neurodegenerative diseases with established mitochondrial pathology, like amyotrophic lateral sclerosis and Chorea Huntington neuroprotective strategies have been suggested. The proposed treatment is buffering of neuronal energy levels by systemic creatine administration. The supplemented creatine passes the blood-brain barrier and increases the total pool of phosphocreatine / creatine available for buffering of the neuronal ATP levels by creatine kinase. Creatine supplementation has been shown to protect motor neurons in a transgenic animal model of amyotrophic lateral sclerosis and striatal neurons in an animal model of Huntingston’s disease. Our NMR spectroscopic data on patients with amyotrophic lateral sclerosis showed upon creatine supplementation increased N-acetyl aspartate levels in the motor cortex of these patients, suggesting at a potential improvement of neuronal energy levels. Interestingly, the buffering of brain energy levels with creatine seems to be effective not only in the mentioned neurodegenerative disorders but also in hypoxia-induced or traumatic brain injury. Moreover, 3 g/kg creatine were observed to reduce hypoxia-induced seizures in rat and rabbit pups. The neuroprotective effect of the creatine treatment in human pathology remains, however, still to be shown.