Objective: The aim of our study is to explore whether nicotinamide adenine dinucleotide (NAD) replenishment could be beneficial on a 6-hydroxydopamine-induced Parkinson’s disease (PD) mouse model and the related mechanisms.

Background: As NAD level declines in PD and its reduction has been reported to be involved in many age-associated neurodegenerative pathologies, we investigated whether NAD could exert a protective role in preventing PD.

Method: To test the above hypothesis, 10 ug 6-hydroxydopamine was injected into right striatum to construct PD mice model and 20 ug NAD was given 4 h before 6-hydroxydopamine. Motor function and dopaminergic neuronal loss in nigrostriatal system were evaluated 4 weeks after surgery. PC12 cells were used to detect the role of NAD against the neurotoxicity caused by 6-hydroxydopamine in cell viability, oxidative stress and mitochondrial functions.

Results: NAD pre-injection in striatum ameliorated the motor deficits and dopaminergic neuronal damage in the substantia nigra and striatum of PD mice. Pre-incubation of NAD protected PC12 cells against cell viability damage, oxidative stress and mitochondrial dysfunction, including decreased mitochondrial numbers and mitochondrial membrane potential, caused by 6-hydroxydopamine.

Conclusion: Our study adds credence to the beneficial role of NAD in preventing parkinsonian neurodegeneration in the PD mice model and suggests that NAD prevents pathological changes in PD via decreasing mitochondrial dysfunctions.

« Back to 2019 International Congress

MDS Abstracts - https://www.mdsabstracts.org/abstract/protective-effects-of-%ce%b2-nicotinamide-adenine-dinucleotide-against-motor-deficits-and-dopaminergic-neuronal-damage-in-a-parkinsons-disease-mouse-model/