Genetic models of Parkinson disease

被引:42
作者
Lim, Kah-Leong [1 ,2 ]
Ng, Chee-Hoe [1 ]
机构
[1] Natl Inst Neurosci, Neurodegenerat Res Lab, Singapore 308433, Singapore
[2] Natl Univ Singapore, Duke NUS Grad Med Sch, Singapore 117548, Singapore
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2009年 / 1792卷 / 07期
基金
英国医学研究理事会;
关键词
Parkinson disease; Synuclein; Parkin; DJ-1; Pink1; LRRK2; MPTP; Neurodegeneration; Dopamine; HUMAN ALPHA-SYNUCLEIN; DOPAMINERGIC NEURON LOSS; UBIQUITIN-PROTEIN LIGASE; DROSOPHILA DJ-1 MUTANTS; RECESSIVE JUVENILE PARKINSONISM; OXIDATIVE STRESS; TRANSGENIC MICE; CAENORHABDITIS-ELEGANS; DJ-1-DEFICIENT MICE; KINASE-ACTIVITY;
D O I
10.1016/j.bbadis.2008.10.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To date, a truly representative animal model of Parkinson disease (PD) remains a critical unmet need. Although toxin-induced PD models have served many useful purposes, they have generally failed to recapitulate accurately the progressive process as well as the nature and distribution of the human pathology. During the last decade or so, the identification of several genes whose mutations are causative of rare familial forms of PD has heralded in a new dawn for PD modelling. Numerous mammalian as well as non mammalian models of genetically-linked PD have since been created. However, despite initial optimism, none of these models turned out to be a perfect replica of PD. Meanwhile, genetic and toxin-induced models alike continue to evolve towards mimicking the disease more faithfully. Notwithstanding this, current genetic models have collectively illuminated several important pathways relevant to PD pathogenesis. Here, we have attempted to provide a comprehensive discussion on existing genetic models of PD. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:604 / 615
页数:12
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