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Collectively, our results suggest that loss of Prdx6 caused by dysregulation of ARE/Nrf2 can be attenuated through a SFN, to combat diseases associated with aging
Surprisingly, optimization using a combination of diet (lower blood glucose and higher blood -hydroxybutyrate), exercise (higher blood lactate), and NAD-related supplementation and modulation of the cytosol-mitochondria NAD-associated reducing equivalents shuttle (hereafter referred to as DEN therapy) increased ATP levels in both neurons and astrocytes toward values of the young metabolic systemcomparable to that of the top-scoring targeted therapy ( Figure 9A
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