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[28] Mitochondrial dysfunction, the other characteristic of secondary brain injury, is also effectively managed by NAC [Figure 6]

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[1] [2] [3] [20] NAD+ supplementation could prevent mitochondrial deterioration and preserve metabolic function/energy (ATP) generation by balancing age-related degradation of NAD+ and its precursor nicotinamide mononucleotide via NADases, particularly CD38