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However, chronic ethanol exposure disrupts autophagic flux, for example, by impairing autophagosomelysosome fusion or by dysregulating key regulators such as mTOR, Beclin-1 and LC3, which leads to the accumulation of dysfunctional mitochondria and toxic protein aggregates [7,35]

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Oral administration of NAD + precursors, such as tryptophan, nicotinic acid (niacin), nicotinamide, and nicotinamide riboside (NR), could increase tissue NAD + levels 525,526

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