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Shan C, Gong YL, Zhuang QQ, et al. Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 2019;94:109670doi: 10.1016/j.pnpbp.2019.109670.
Shan, C., Gong, Y. L., Zhuang, Q. Q., Hou, Y. F., Wang, S. M., Zhu, Q., Huang, G. R., Tao, B., Sun, L. H., Zhao, H. Y., Li, S. T., & Liu, J. M. (2019). Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease. Progress in neuro-psychopharmacology & biological psychiatry, 94109670. https://doi.org/10.1016/j.pnpbp.2019.109670
Shan, Chang, et al. "Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease." Progress in neuro-psychopharmacology & biological psychiatry vol. 94 (2019): 109670. doi: https://doi.org/10.1016/j.pnpbp.2019.109670
Shan C, Gong YL, Zhuang QQ, Hou YF, Wang SM, Zhu Q, Huang GR, Tao B, Sun LH, Zhao HY, Li ST, Liu JM. Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease. Prog Neuropsychopharmacol Biol Psychiatry. 2019 Aug 30;94:109670. doi: 10.1016/j.pnpbp.2019.109670. Epub 2019 Jun 17. PMID: 31220519.
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Prog Neuropsychopharmacol Biol Psychiatry. 2019 Aug 30;94:109670. doi: 10.1016/j.pnpbp.2019.109670. Epub 2019 Jun 17.

Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease.

Progress in neuro-psychopharmacology & biological psychiatry

Chang Shan, Yan-Ling Gong, Qian-Qian Zhuang, Yan-Fang Hou, Shu-Min Wang, Qin Zhu, Guo-Rui Huang, Bei Tao, Li-Hao Sun, Hong-Yan Zhao, Sheng-Tian Li, Jian-Min Liu

Affiliations

  1. Department of Endocrine and Metabolic Diseases, Rui-jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases. Shanghai 200025, China.
  2. Bio-X Institutes, Key laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Key Laboratory of Psychotic Disorders, Brain Science and Technology Research Center, Shanghai Jiao Tong University, Shanghai 200240, China.
  3. Bio-X Institutes, Key laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Key Laboratory of Psychotic Disorders, Brain Science and Technology Research Center, Shanghai Jiao Tong University, Shanghai 200240, China. Electronic address: [email protected].
  4. Department of Endocrine and Metabolic Diseases, Rui-jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases. Shanghai 200025, China. Electronic address: [email protected].

PMID: 31220519 DOI: 10.1016/j.pnpbp.2019.109670

Abstract

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.

Copyright © 2019 Elsevier Inc. All rights reserved.

Keywords: Dopaminergic neuronal damage; Mitochondrial dysfunction; Oxidative stress; Parkinson's disease; β-Nicotinamide adenine dinucleotide

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