Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
复制标题
DOI：
10.1002/mds.25108
复制
发表时间：
2013-01
影响因子：
8.6
通讯作者：
Spillantini, Maria Grazia
中科院分区：
文献类型：
--
作者：
Bezard, Erwan;Yue, Zhenyu;Kirik, Deniz;Spillantini, Maria Grazia
在过去的二十年中，人们对帕金森病（PD）的病因和发病机制有了更深入的了解。实验模型对于更深入地了解疾病的发病机制至关重要。到目前为止，基于神经毒素的动物模型是体外和体内系统中产生选择性神经元死亡的最流行的工具。这些模型通常被称为致病模型。目前PD建模的趋势围绕着所谓的基于疾病基因的模型或病因学模型。利用具有不同损伤机制的多种模型的价值在于，产生多巴胺（DA）的神经元死于刻板级联反应，这种级联反应可被一系列损伤激活，从神经毒素到疾病相关基因的下调和过表达。在这篇立场论文中，我们提出了病原学和病原学模型的相关性，以及临床相关设计的概念，我们认为在进入临床试验之前，应该在新的神经保护疗法的临床前开发阶段利用这些概念。
Over the last two decades significant strides has been made towards acquiring a better knowledge of both the aetiology and pathogenesis of Parkinson’s disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modelling PD revolves around what can be called the disease gene-based models, or etiologic models. The value of utilizing multiple models with different mechanism of insult rests on the premise that dopamine (DA) producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to down-regulation and overexpression of disease-related genes. In this position paper, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that we argue should be utilized in the pre-clinical development phase of new neuroprotective therapies before embarking into clinical trials.
登录
查看更多内容
影响因子：
15.1
作者：
Daher JP;Ying M;Banerjee R;McDonald RS;Hahn MD;Yang L;Flint Beal M;Thomas B;Dawson VL;Dawson TM;Moore DJ
通讯作者：
Moore DJ
影响因子：
14.5
作者：
Eslamboli, Andisheh;Romero-Ramos, Marina;Kirik, Deniz
通讯作者：
Kirik, Deniz
影响因子：
2.5
作者：
Crowther, RA;Daniel, SE;Goedert, M
通讯作者：
Goedert, M
影响因子：
2.9
作者：
Björklund, A;Kirik, D;Mandel, RJ
通讯作者：
Mandel, RJ
影响因子：
6.1
作者：
Decressac, M.;Mattsson, B.;Bjorklund, A.
通讯作者：
Bjorklund, A.