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MPTP 帕金森病动物模型在转化医学中的应用

MPTP Mouse Model of Preclinical and Clinical Parkinson's Disease as an Instrument for Translational Medicine.

机构信息

Laboratory of Neural and Neuroendocrine Regulations, Institute of Developmental Biology RAS, 26, Vavilov St., Moscow, Russia, 119334.

Laboratory of Pharmacoproteomics, Institute of Biomedical Chemistry RAS, 10 Building 8, Pogodinskaya St, Moscow, Russia, 119121.

出版信息

Mol Neurobiol. 2018 Apr;55(4):2991-3006. doi: 10.1007/s12035-017-0559-6. Epub 2017 Apr 29.

Abstract

Parkinson's disease (PD) is characterized by the appearance of motor symptoms many years after the onset of neurodegeneration, which explains low efficiency of therapy. Therefore, one of the priorities in neurology is to develop an early diagnosis and preventive treatment of PD, based on knowledge of molecular mechanisms of neurodegeneration and neuroplasticity in the nigrostriatal system. However, due to inability to diagnose PD at preclinical stage, research and development must be performed in animal models by comparing the nigrostriatal system in the models of asymptomatic and early symptomatic stages of PD. In this study, we showed that despite the progressive loss of neurons in the substantia nigra at the presymptomatic and symptomatic stage, almost no change was observed in the main functional characteristics of this brain region, including dopamine (DA) uptake and release, dopamine transporter (DAT) and vesicular monoamine transporter 2 (VMAT2) expression, and activity of MAO-A and MAO-B. In the striatum of presymptomatic mice, some parameters (DA release and uptake, MAO-A activity) remained compensatory unchanged or compensatory decreased (MAO-B gene expression and activity), while others-a reduction in DA levels in tissue and extracellular space and in VMAT2 and DAT expression-manifest the functional failure. In symptomatic mice, only a few parameters (spontaneous DA release and uptake, MAO-B gene expression and activity) remained at the same level as at presymptomatic stage, while most parameters (DA level in tissue and extracellular space, DA-stimulated release, VMAT2 and DAT contents), decreased, showing decompensation, which was enhanced by increasing MAO-A activity. Thus, this study provides a comprehensive assessment of the molecular mechanisms of neuroplasticity in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine models of preclinical and clinical stages of PD, which could potentially serve as a powerful tool for translational medicine.

摘要

帕金森病(PD)的特征是神经退行性变发生多年后才出现运动症状,这解释了治疗效果不佳的原因。因此,神经病学的优先事项之一是基于对黑质纹状体系统神经退行性变和神经可塑性的分子机制的了解,开发 PD 的早期诊断和预防性治疗。然而,由于无法在临床前阶段诊断 PD,因此必须在动物模型中进行研究和开发,方法是比较 PD 无症状和早期有症状阶段的黑质纹状体系统。在这项研究中,我们表明,尽管在无症状和有症状阶段前体神经元逐渐丧失,但该脑区的主要功能特征几乎没有变化,包括多巴胺(DA)摄取和释放、多巴胺转运体(DAT)和囊泡单胺转运体 2(VMAT2)的表达以及 MAO-A 和 MAO-B 的活性。在无症状小鼠的纹状体中,一些参数(DA 释放和摄取、MAO-A 活性)保持代偿性不变或代偿性降低(MAO-B 基因表达和活性),而其他参数-组织和细胞外空间中 DA 水平以及 VMAT2 和 DAT 表达的降低-表现出功能衰竭。在有症状的小鼠中,只有少数参数(自发 DA 释放和摄取、MAO-B 基因表达和活性)与无症状阶段保持相同水平,而大多数参数(组织和细胞外空间中的 DA 水平、DA 刺激释放、VMAT2 和 DAT 含量)下降,表现出失代偿,这因 MAO-A 活性的增加而加剧。因此,这项研究全面评估了 1-甲基-4-苯基-1,2,3,6-四氢吡啶临床前和临床阶段 PD 模型中神经可塑性的分子机制,这可能成为转化医学的有力工具。

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