Journal
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Volume 94, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pnpbp.2019.109670
Keywords
beta-Nicotinamide adenine dinucleotide; Parkinson's disease; Dopaminergic neuronal damage; Oxidative stress; Mitochondrial dysfunction
Funding
- National Natural Science Foundation of China [81870619, 81570796, 81871064]
- National Key Research and Development Program of China [2016YFC1201701]
- Shanghai Committee of Science and Technology [13dz2260500]
- Innovation Program of Shanghai Municipal Education Commission [2019-01-07-00-02-E00037]
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The level of nicotinamide adenine dinucleotide (NAD) decreases in Parkinson's disease (PD), and its reduction has been reported to be involved in many age-associated neurodegenerative pathologies. Thus, we investigated whether NAD replenishment is beneficial in a 6-hydroxydopamine (6-OHDA)-induced mouse model of PD. Preinjection with NAD in the striatum ameliorated motor deficits and dopaminergic neuronal damage in the substantia nigra and striatum of a mouse model of PD. Moreover, preincubation with NAD protected PC12 cells against the loss of cell viability, morphological damage, oxidative stress and mitochondrial dysfunction caused by 6-OHDA. These results add credence to the beneficial role of NAD against parkinsonian neurodegeneration in mouse models of PD, provide evidence for the potential of NAD for the prevention of PD, and suggest that NAD prevents pathological changes in PD via decreasing mitochondrial dysfunctions.
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