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518 Furthermore, increasing the level of available NAD + by supplementing diet containing NAD + precursors or inhibiting the activity of NAD + -dependent enzyme (e.g., PARP that snatches NAD + competing with mitochondria) is a feasible strategy to avoid the neurotoxicity related to mitochondrial dysfunction

Front Psychiatry 9 , 767 (2018)

MitoQ, a ubiquinone derivative that targets mitochondria, was found to restore the significant disruption in mitochondrial morphology and function induced by RSL3 (a small molecule that induces ferroptosis) [85]

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But for patients, the situation is far less fortunate