Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Nicotinamide Mononucleotide (NMN) is a precursor to nicotinamide adenine dinucleotide (NAD+), an essential molecule involved in cellular metabolism and energy production. Scientific interest in NMN for nerve damage arises from preclinical evidence suggesting that boosting NAD+ levels can promote neuronal survival and axonal regeneration. Several animal studies have demonstrated that NMN supplementation restores NAD+ levels and mitigates neurodegeneration or nerve injury in models of peripheral neuropathy and central nervous system damage. For example, research in rodents has shown that NMN administration can delay axonal degeneration after sciatic nerve injury and protect against chemotherapy-induced peripheral neuropathy. These effects are thought to be mediated through enhanced mitochondrial function, reduced oxidative stress, and activation of sirtuin pathways implicated in neuronal survival. However, as of June 2024, robust clinical evidence in humans is lacking. Most of the supportive data comes from animal or in vitro studies, and results from human trials targeting nerve damage are either absent or very preliminary. The evidence base is therefore limited and does not yet establish NMN as a proven treatment for nerve damage in humans. No major clinical guidelines currently recommend NMN for this purpose. Thus, while there is scientific rationale and preclinical evidence, human data are insufficient, and the overall evidence level is low to moderate (rated 2 out of 5).

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