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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-gila 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.

The thiopurines are routinely administered to patients of various clinical conditions. After metabolism to thiopurine nucleotides, 6-mercatopurine (6-MP), azathioprine (AZA) and 6-thioguanine (6-TG) exert cytotoxicity as inactive pro-drugs. 6-MP is catabolized through xanthine oxidase and methylation catalyzed by thiopurine methyltransferase (TPMT). 6-MP serves as maintenance treatment for acute lymphoblastic leukemia.