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热量限制可提高神经营养因子水平,并减轻帕金森病灵长类动物模型中的神经化学和行为缺陷。

Caloric restriction increases neurotrophic factor levels and attenuates neurochemical and behavioral deficits in a primate model of Parkinson's disease.

作者信息

Maswood Navin, Young Jennifer, Tilmont Edward, Zhang Zhiming, Gash Don M, Gerhardt Greg A, Grondin Richard, Roth George S, Mattison Julie, Lane Mark A, Carson Richard E, Cohen Robert M, Mouton Peter R, Quigley Christopher, Mattson Mark P, Ingram Donald K

机构信息

Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.

出版信息

Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18171-6. doi: 10.1073/pnas.0405831102. Epub 2004 Dec 16.

DOI:10.1073/pnas.0405831102
PMID:15604149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC539733/
Abstract

We report that a low-calorie diet can lessen the severity of neurochemical deficits and motor dysfunction in a primate model of Parkinson's disease. Adult male rhesus monkeys were maintained for 6 months on a reduced-calorie diet [30% caloric restriction (CR)] or an ad libitum control diet after which they were subjected to treatment with a neurotoxin to produce a hemiparkinson condition. After neurotoxin treatment, CR monkeys exhibited significantly higher levels of locomotor activity compared with control monkeys as well as higher levels of dopamine (DA) and DA metabolites in the striatal region. Increased survival of DA neurons in the substantia nigra and improved manual dexterity were noted but did not reach statistical significance. Levels of glial cell line-derived neurotrophic factor, which is known to promote the survival of DA neurons, were increased significantly in the caudate nucleus of CR monkeys, suggesting a role for glial cell line-derived neurotrophic factor in the anti-Parkinson's disease effect of the low-calorie diet.

摘要

我们报告称,在帕金森病的灵长类动物模型中,低热量饮食可减轻神经化学缺陷和运动功能障碍的严重程度。成年雄性恒河猴分别采用低热量饮食[30%热量限制(CR)]或随意进食的对照饮食喂养6个月,之后用神经毒素进行处理以诱发偏侧帕金森病状态。神经毒素处理后,与对照猴相比,CR猴表现出显著更高水平的运动活性,以及纹状体区域中更高水平的多巴胺(DA)和DA代谢产物。黑质中DA神经元的存活率增加以及手部灵活性改善,但未达到统计学显著性。已知可促进DA神经元存活的胶质细胞源性神经营养因子水平在CR猴的尾状核中显著升高,这表明胶质细胞源性神经营养因子在低热量饮食的抗帕金森病作用中发挥了作用。

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