Therapeutic potential of the nutraceutical nicotinamide mononucleotide to treat early‐life stress‐induced emotional and metabolic alterations


Our overarching hypothesis is that the behavioral reprogramming induced by peripubertal stress is mediated by decreased signaling of the adipokine eNampt and subsequent impairment of the NAD+/SIRT1 pathway in the NAc. Therefore, our specific hypothesis 1 is that Sirt1 overexpression in the nucleus accumbens (NAc) or normalization of plasmatic levels of eNampt would revert the stressinduced behavioral alterations. Our specific hypothesis 2 is that a nutritional intervention with the NAD+-boosting compound NMN would prevent the alterations in brain and behavior exhibited by stressed mice. We will test our hypotheses through two main objectives :

Objective 1

To evaluate whether decreased eNampt levels and impaired SIRT1 signaling in the NAc underlie the behavioral alterations exhibited by peripubertal stressed mice

Objective 2

To test the therapeutic potential of the NAD+-boosting compound NMN to counteract the negative impact of early life-stress on brain function and behavior

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