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By inhibiting NNMT, 5-Amino-1MQ may spare nicotinamide for NAD+ synthesis via the salvage pathway, thereby activating SIRT1 (Sirtuin 1) pathways associated with mitochondrial biogenesis, fat oxidation, and metabolic flexibility [3]

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Similarly, human plasma studies in patients with ASD have demonstrated abnormal branched-chain amino acid levels (105), while transfection of mice with microorganisms from these individuals has also led to behavioral changes in mice in multiple studies (104, 107)

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