Nicotinamide Mononucleotide (NMN) is a precursor to nicotinamide adenine dinucleotide (NAD+), a crucial coenzyme in cellular energy metabolism and mitochondrial function. Interest in NMN as a supportive therapy for Parkinson’s Disease (PD) stems from preclinical studies indicating that NAD+ metabolism may play a role in neurodegeneration. Some animal studies, such as those involving mouse models of PD, have shown that boosting NAD+ levels via NMN administration can improve mitochondrial function and reduce neuronal damage. These findings are linked to the hypothesis that impaired mitochondrial bioenergetics and oxidative stress contribute to PD pathology, and thus, enhancing NAD+ supply might offer neuroprotection.

However, as of June 2024, there is no robust clinical evidence in humans to support the use of NMN for treating or significantly altering the course of Parkinson’s Disease. Most data are limited to cell culture and animal models, with only a handful of small, early-phase human trials examining NMN’s safety and general effects on aging, not specifically PD. No major clinical guidelines recommend NMN for PD, and it is not a standard or approved therapy for this condition. The current scientific evidence, while intriguing, remains preliminary and insufficient to justify routine use in PD patients.

In summary, NMN’s use in Parkinson’s Disease is supported by early-stage scientific investigation, but clear clinical benefits in humans have yet to be demonstrated.