Synopsis

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

Nicotinamide Mononucleotide (NMN) is a precursor to nicotinamide adenine dinucleotide (NAD+), a coenzyme involved in cellular metabolism and energy production. Recent scientific interest has focused on NMN as a potential therapeutic agent for neurodegenerative diseases, including dementia. Preclinical studies, primarily in animal models, suggest that NMN supplementation can increase NAD+ levels in the brain, potentially improving mitochondrial function, reducing neuroinflammation, and enhancing neuronal survival. These effects are relevant since NAD+ levels decline with age and are implicated in cognitive decline and neurodegeneration.

Several animal studies have shown that NMN administration can improve cognitive function and reduce pathological features in models of Alzheimer’s disease and other dementias. Mechanistic data suggest benefits through improved DNA repair, reduced oxidative stress, and enhanced synaptic plasticity. However, evidence in humans is minimal. Early-phase clinical trials have demonstrated that NMN supplementation is generally safe and can increase NAD+ levels, but robust clinical data showing cognitive benefit in dementia patients are lacking. No large randomized controlled trials have conclusively demonstrated efficacy for dementia treatment or prevention.

In summary, while the use of NMN for dementia is scientifically inspired and supported by promising preclinical results, the clinical evidence remains limited. Thus, this use is justified by early scientific research rather than tradition, with the current level of evidence best rated as low to moderate (2/5) pending further human studies.

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