Animal models of PD: Pieces of the same puzzle?

被引：114

作者：

Dawson, TM ^{[1
]}

Mandir, AS

Lee, MK

机构：

[1] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21287 USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA

[3] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21287 USA

[4] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21287 USA

来源：

NEURON | 2002年 / 35卷 / 02期

关键词：

D O I：

10.1016/S0896-6273(02)00780-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Parkinson's disease (PD) is a common neurodegenerative disorder with no known cure. The etiology of PD is likely due, in part, to combinations of genetic susceptibilities and environmental factors. In rare familial cases, PD is due to genetic mutations. A number of new genetic and toxin models of PD and advances in older models are yielding important new information about the pathogenesis of PD. This has prompted us to critically review the current animal models for PD and discuss how these models may yield fresh insights into the pathogenesis of PD, as well as new therapeutic opportunities.

引用

页码：219 / 222

页数：4

共 20 条

[1] Chaperone suppression of α-synuclein toxicity in a Drosophila model for Parkinson's disease [J].

Auluck, PK ;

Chan, HYE ;

Trojanowski, JQ ;

Lee, VMY ;

Bonini, NM .

SCIENCE, 2002, 295 (5556) :865-868

[2] Experimental models of Parkinson's disease [J].

Beal, MF .

NATURE REVIEWS NEUROSCIENCE, 2001, 2 (05) :325-332

[3] Chronic systemic pesticide exposure reproduces features of Parkinson's disease [J].

Betarbet, R ;

Sherer, TB ;

MacKenzie, G ;

Garcia-Osuna, M ;

Panov, AV ;

Greenamyre, JT .

NATURE NEUROSCIENCE, 2000, 3 (12) :1301-1306

[4] Prospects for new restorative and neuroprotective treatments in Parkinson's disease [J].

Dunnett, SB ;

Björklund, A .

NATURE, 1999, 399 (6738) :A32-A39

[5] A Drosophila model of Parkinson's disease [J].

Feany, MB ;

Bender, WW .

NATURE, 2000, 404 (6776) :394-398

[6] Neuronal α-synucleinopathy with severe movement disorder in mice expressing A53T human α-synuclein [J].

Giasson, BI ;

Duda, JE ;

Quinn, SM ;

Zhang, B ;

Trojanowski, JQ ;

Lee, VMY .

NEURON, 2002, 34 (04) :521-533

[7] Alpha-synuclein and neurodegenerative diseases [J].

Goedert, M .

NATURE REVIEWS NEUROSCIENCE, 2001, 2 (07) :492-501

[8] β-synuclein inhibits α-synuclein aggregation:: A possible role as an anti-parkinsonian factor [J].

Hashimoto, M ;

Rockenstein, E ;

Mante, M ;

Mallory, M ;

Masliah, E .

NEURON, 2001, 32 (02) :213-223

[9] Parkinson-like neurodegeneration induced by targeted overexpression of α-synuclein in the nigrostriatal system [J].

Kirik, D ;

Rosenblad, C ;

Burer, C ;

Lundberg, C ;

Johansen, TE ;

Muzyczka, N ;

Mandel, RJ ;

Björklund, A .

JOURNAL OF NEUROSCIENCE, 2002, 22 (07) :2780-2791

[10] Genetics of Parkinson's disease and biochemical studies of implicated gene products [J].

Lansbury, PT ;

Brice, A .

CURRENT OPINION IN GENETICS & DEVELOPMENT, 2002, 12 (03) :299-306

← 1 2 →