Molecular Neurobiology, Institute of Life Science, Medical School, Swansea University, UK.
Biomedicine Discovery Institute & Department of Physiology, Monash University, Melbourne, Victoria, Australia.
Neuropharmacology. 2018 Jul 1;136(Pt B):317-326. doi: 10.1016/j.neuropharm.2017.12.027. Epub 2017 Dec 23.
Parkinson's disease is a common age-related neurodegenerative disorder affecting 10 million people worldwide, but the mechanisms underlying its pathogenesis are still unclear. The disease is characterised by dopamine nerve cell loss in the mid-brain and intra-cellular accumulation of α-synuclein that results in motor and non-motor dysfunction. In this review, we discuss the neuroprotective effects of the stomach hormone, ghrelin, in models of Parkinson's disease. Recent findings suggest that it may modulate mitochondrial function and autophagic clearance of impaired organelle in response to changes in cellular energy balance. We consider the putative cellular mechanisms underlying ghrelin-action and the possible role of ghrelin mimetics in slowing or preventing Parkinson's disease progression. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'
帕金森病是一种常见的与年龄相关的神经退行性疾病，影响全球 1000 万人，但发病机制仍不清楚。该疾病的特征是中脑多巴胺神经细胞丧失和α-突触核蛋白在细胞内积聚，导致运动和非运动功能障碍。在这篇综述中，我们讨论了胃激素 ghrelin 在帕金森病模型中的神经保护作用。最近的研究结果表明，它可能调节线粒体功能和自噬清除受损细胞器，以响应细胞能量平衡的变化。我们考虑了 ghrelin 作用的潜在细胞机制以及 ghrelin 类似物在减缓或预防帕金森病进展中的可能作用。本文是题为“代谢损伤作为神经退行性疾病风险因素”的特刊的一部分。
