| dc.description.abstract | Parkinson’s disease (PD) is a common age-related neurodegenerative disorder, with a rapidly increasing age-dependent prevalence. Current treatment offers some symptomatic relief but has no effect on disease progression. Thus, developing a drug that can slow down or alter the progression of the disease is greatly needed. In recent years, boosting of nicotinamide adenine dinucleotide (NAD) has gained a lot of attention as a potential intervention to stall PD progression. NAD is an essential and naturally occurring molecule in our body; however, it has been reported to decline with age and its depletion has been linked to pathological pathways found in PD. Nicotinamide mononucleotide (NMN) is the direct precursor in NAD biosynthesis and orally available as supplement to increase NAD. However, many aspects still remain unknown regarding such supplementation, including the rate and extent of NAD increase and decrease following oral NMN supplementation and discontinuation, respectively, especially with regard to its impact on brain NAD levels. This study aimed to determine the simultaneous change in blood and brain NAD levels following oral NMN supplementation in six healthy volunteers. Results showed that whole blood NAD levels increased slowly but significantly during NMN supplementation, and gradually returned to baseline levels following discontinuation. Cerebral NAD levels were measured by 31Phosphorous magnetic resonance spectroscopy (31P-MRS), and showed no apparent effect of the supplemented NMN, which could be, in part, due to rather noisy brain data. Interindividual differences in NAD levels were observed at baseline and throughout the study period, but no associations of the NMN response with regard to demographic factors such as sex, weight or age were observed. Although NMN successfully elevated blood NAD levels gradually over several days, further studies are needed to also detect clear changes in the brain. | |
