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Further, the NADH from increased glycolysis in the cytosol can be transferred to mitochondria to drive NADH-dependent NNT

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Pre-clinical studies also suggest mechanisms occurring within the GABA metabolic shunt, such as the modulation of the calcium ion channel blockade of the monoamine oxidase-B receptor substrate, thereby inhibiting glutamate and promoting GABA synthesis [70,81,82,83]

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