Modelling of Parkinson's disease in mice

被引:145
作者
Chesselet, Marie-Francoise [1 ]
Richter, Franziska [1 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA
基金
美国国家卫生研究院;
关键词
HUMAN ALPHA-SYNUCLEIN; TRANSGENIC MICE; MOTOR DEFICITS; MOUSE MODELS; WILD-TYPE; MITOCHONDRIAL DYSFUNCTION; DOPAMINE RELEASE; ANIMAL-MODELS; MUTANT; LRRK2;
D O I
10.1016/S1474-4422(11)70227-7
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Although progress has been made in the symptomatic treatment of Parkinson's disease since the discovery of L-dopa in the 1960s, no neuroprotective therapy is yet available. Absence of adequate animal models of the disease that enable prediction of clinical success of potential treatments is often cited as a major impediment to progress and discourages researchers and pharmaceutical companies from investing resources to develop such treatments. Classic models are still widely used, but have been disappointing, and development of genetic models has given new hope. However, can a human disease be faithfully reproduced in a mouse? In this Review we summarise evidence that some genetic mouse models do reproduce key features of Parkinson's disease and show that much can be learned from even imperfect models. The hope is that this information could be used to advance the search for neuroprotective therapies for Parkinson's disease.
引用
收藏
页码:1108 / 1118
页数:11
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