Animal models of PD: Pieces of the same puzzle?

被引:113
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
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
收藏
页码:219 / 222
页数:4
相关论文
共 20 条
  • [11] Advances in genetic models of Parkinson's disease
    Lee, MK
    Price, DL
    [J]. CLINICAL NEUROSCIENCE RESEARCH, 2001, 1 (06) : 456 - 466
  • [12] Human α-synuclein-harboring familial Parkinson's disease-linked Ala-53→Thr mutation causes neurodegenerative disease with α-synuclein aggregation in transgenic mice
    Lee, MK
    Stirling, W
    Xu, YQ
    Xu, XY
    Qui, D
    Mandir, AS
    Dawson, TM
    Copeland, NG
    Jenkins, NA
    Price, DL
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (13) : 8968 - 8973
  • [13] The herbicide paraquat causes up-regulation and aggregation of α-synuclein in mice -: Paraquat and α-synuclein
    Manning-Bog, AB
    McCormack, AL
    Li, J
    Uversky, VN
    Fink, AL
    Di Monte, DA
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (03) : 1641 - 1644
  • [14] β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease
    Masliah, E
    Rockenstein, E
    Veinbergs, I
    Sagara, Y
    Mallory, M
    Hashimoto, M
    Mucke, L
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (21) : 12245 - 12250
  • [15] Dopaminergic loss and inclusion body formation in α-synuclein mice:: Implications for neurodegenerative disorders
    Masliah, E
    Rockenstein, E
    Veinbergs, I
    Mallory, M
    Hashimoto, M
    Takeda, A
    Sagara, Y
    Sisk, A
    Mucke, L
    [J]. SCIENCE, 2000, 287 (5456) : 1265 - 1269
  • [16] Behavioral and neurochemical effects of wild-type and mutated human α-synuclein in transgenic mice
    Richfield, EK
    Thiruchelvam, MJ
    Cory-Slechta, DA
    Wuertzer, C
    Gainetdinov, RR
    Caron, MG
    Di Monte, DA
    Federoff, HJ
    [J]. EXPERIMENTAL NEUROLOGY, 2002, 175 (01) : 35 - 48
  • [17] Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila
    Steffan, JS
    Bodai, L
    Pallos, J
    Poelman, M
    McCampbell, A
    Apostol, BL
    Kazantsev, A
    Schmidt, E
    Zhu, YZ
    Greenwald, M
    Kurokawa, R
    Housman, DE
    Jackson, GR
    Marsh, JL
    Thompson, LM
    [J]. NATURE, 2001, 413 (6857) : 739 - 743
  • [18] Thiruchelvam M, 2000, J NEUROSCI, V20, P9207
  • [19] Neuropathology in mice expressing human α-synuclein
    van der Putten, H
    Wiederhold, KH
    Probst, A
    Barbieri, S
    Mistl, C
    Danner, S
    Kauffmann, S
    Hofele, K
    Spooren, WPJM
    Ruegg, MA
    Lin, S
    Caroni, P
    Sommer, B
    Tolnay, M
    Bilbe, G
    [J]. JOURNAL OF NEUROSCIENCE, 2000, 20 (16) : 6021 - 6029
  • [20] Dopamine-dependent neurotoxicity of α-synuclein:: A mechanism for selective neurodegeneration in Parkinson disease
    Xu, J
    Kao, SY
    Lee, FJS
    Song, WH
    Jin, LW
    Yankner, BA
    [J]. NATURE MEDICINE, 2002, 8 (06) : 600 - 606