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Neuroprotective potential of Quercetin in combination with piperine against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity.槲皮素与胡椒碱联合使用对1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的神经毒性的神经保护潜力。
Neural Regen Res. 2017 Jul;12(7):1137-1144. doi: 10.4103/1673-5374.211194.
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Beneficial effect of antidepressants against rotenone induced Parkinsonism like symptoms in rats.抗抑郁药对鱼藤酮诱导的大鼠帕金森氏症样症状的有益作用。
Pathophysiology. 2016 Jun;23(2):123-34. doi: 10.1016/j.pathophys.2016.03.002. Epub 2016 Mar 15.
3
L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway.L-茶氨酸,绿茶的一种成分,通过调节一氧化氮途径预防3-硝基丙酸(3-NP)诱导的纹状体毒性。
Mol Neurobiol. 2017 Apr;54(3):2327-2337. doi: 10.1007/s12035-016-9822-5. Epub 2016 Mar 9.
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Antidepressants for neuroprotection in Huntington's disease: A review.用于亨廷顿舞蹈症神经保护的抗抑郁药:综述
Eur J Pharmacol. 2015 Dec 15;769:33-42. doi: 10.1016/j.ejphar.2015.10.033. Epub 2015 Oct 25.
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Parallel basal ganglia circuits for voluntary and automatic behaviour to reach rewards.用于追求奖励的自愿和自动行为的平行基底神经节回路。
Brain. 2015 Jul;138(Pt 7):1776-800. doi: 10.1093/brain/awv134. Epub 2015 May 16.
6
Phosphodiesterases: Regulators of cyclic nucleotide signals and novel molecular target for movement disorders.磷酸二酯酶:环核苷酸信号的调节剂和运动障碍的新型分子靶点。
Eur J Pharmacol. 2013 Aug 15;714(1-3):486-97. doi: 10.1016/j.ejphar.2013.06.038. Epub 2013 Jul 10.
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Dopamine imbalance in Huntington's disease: a mechanism for the lack of behavioral flexibility.亨廷顿病中的多巴胺失衡:行为灵活性缺乏的一种机制。
Front Neurosci. 2013 Jul 4;7:114. doi: 10.3389/fnins.2013.00114. eCollection 2013.
8
Neurosteroid and neurotransmitter alterations in Parkinson's disease.帕金森病中的神经甾体和神经递质改变。
Front Neuroendocrinol. 2013 Apr;34(2):132-42. doi: 10.1016/j.yfrne.2013.03.001. Epub 2013 Apr 4.
9
Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 mice.尽管全长 BACHD 和 YAC128 小鼠具有相似的行为和神经病理学特征,但神经化学和聚集物存在明显差异。
Hum Mol Genet. 2012 May 15;21(10):2219-32. doi: 10.1093/hmg/dds037. Epub 2012 Feb 9.
10
GABA-B receptor: possible target for Parkinson's disease therapy.γ-氨基丁酸B受体:帕金森病治疗的潜在靶点。
Exp Neurol. 2012 Jan;233(1):121-2. doi: 10.1016/j.expneurol.2011.10.012. Epub 2011 Oct 25.

纹状体神经递质在帕金森病和亨廷顿病发病机制中的新作用研究进展:综述。

Insight Into the Emerging Role of Striatal Neurotransmitters in the Pathophysiology of Parkinson's Disease and Huntington's Disease: A Review.

机构信息

School of Pharmacy and Emerging Sciences, Baddi University of Emerging Sciences & Technology, Baddi, Solan, India.

Department of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Panjab, India.

出版信息

Curr Neuropharmacol. 2019;17(2):165-175. doi: 10.2174/1570159X16666180302115032.

DOI:10.2174/1570159X16666180302115032
PMID:29512464
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6343208/
Abstract

Alteration in neurotransmitters signaling in basal ganglia has been consistently shown to significantly contribute to the pathophysiological basis of Parkinson's disease and Huntington's disease. Dopamine is an important neurotransmitter which plays a critical role in coordinated body movements. Alteration in the level of brain dopamine and receptor radically contributes to irregular movements, glutamate mediated excitotoxic neuronal death and further leads to imbalance in the levels of other neurotransmitters viz. GABA, adenosine, acetylcholine and endocannabinoids. This review is based upon the data from clinical and preclinical studies to characterize the role of various striatal neurotransmitters in the pathogenesis of Parkinson's disease and Huntington's disease. Further, we have collected data of altered level of various neurotransmitters and their metabolites and receptor density in basal ganglia region. Although the exact mechanisms underlying neuropathology of movement disorders are not fully understood, but several mechanisms related to neurotransmitters alteration, excitotoxic neuronal death, oxidative stress, mitochondrial dysfunction, neuroinflammation are being put forward. Restoring neurotransmitters level and downstream signaling has been considered to be beneficial in the treatment of Parkinson's disease and Huntington's disease. Therefore, there is an urgent need to identify more specific drugs and drug targets that can restore the altered neurotransmitters level in brain and prevent/delay neurodegeneration.

摘要

基底神经节中神经递质信号的改变被一致证明对帕金森病和亨廷顿病的病理生理基础有重要贡献。多巴胺是一种重要的神经递质,在协调身体运动中起着关键作用。大脑多巴胺和受体水平的改变极大地导致了不规则运动、谷氨酸介导的兴奋性神经元死亡,并进一步导致其他神经递质(如 GABA、腺苷、乙酰胆碱和内源性大麻素)水平失衡。本综述基于临床和临床前研究的数据,描述了各种纹状体神经递质在帕金森病和亨廷顿病发病机制中的作用。此外,我们还收集了基底神经节区域各种神经递质及其代谢物和受体密度改变的相关数据。虽然运动障碍神经病理学的确切机制尚未完全阐明,但目前提出了几种与神经递质改变、兴奋性神经元死亡、氧化应激、线粒体功能障碍、神经炎症相关的机制。恢复神经递质水平和下游信号转导被认为对治疗帕金森病和亨廷顿病有益。因此,迫切需要确定更具特异性的药物和药物靶点,以恢复大脑中改变的神经递质水平,并预防/延缓神经退行性变。