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The central clinical idea: when mitochondrial ATP production falls and oxidative stress rises, the brain may lose the energy and antioxidant reserve needed to regulate neurotransmission, maintain cell membranes, recycle methionine, produce SAM, clear adenosine and homocysteine, build glutathione and tolerate medications or supplements

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Taking proactive steps towards prevention can be a sensible way to avoid this issue

Additionally, the amount of medication given was inconsistent

Functionally, through this interaction, D2R recruits DAT to plasma membrane and therefore enhances the reuptake of dopamine