Transgenic invertebrate models of age-associated neurodegenerative diseases

被引:77
作者
Link, CD [1 ]
机构
[1] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA
关键词
neurodegeneration; transgenic; Drosophila; Caenorhabditis; polyglutamine; Alzheimer's disease;
D O I
10.1016/S0047-6374(01)00291-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Transgenic Drosophila melanogaster and Caenorhabditis elegans strains have been engineered to express human proteins associated with neurodegenerative diseases. These model systems include transgenic animals expressing beta-amyloid peptide (Alzheimer's disease), polyglutamine repeat proteins (Huntington's disease, Spinocerebellar ataxia), and alpha-synuclein (Parkinson's disease). In most of these invertebrate models, some aspects of the human diseases are reproduced, Although expression of all these proteins in transgenic mice has been instructive, the invertebrate models offer experimental advantages (e.g. forward genetic screens) that can potentially address some of the outstanding questions regarding the cellular processes underlying these diseases. This review considers what has been learned from these invertebrate models, and speculates what further insight may be gained from them. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:1639 / 1649
页数:11
相关论文
共 25 条
[1]   Mechanisms of chaperone suppression of polyglutamine disease:: selectivity, synergy and medullation of protein solubility in Drosophila [J].
Chan, HYE ;
Warrick, JM ;
Gray-Board, GL ;
Paulson, HL ;
Bonini, NM .
HUMAN MOLECULAR GENETICS, 2000, 9 (19) :2811-2820
[2]   Drosophila models of human neurodegenerative disease [J].
Chan, HYE ;
Bonini, NM .
CELL DEATH AND DIFFERENTIATION, 2000, 7 (11) :1075-1080
[3]   Oxidation versus aggregation - how do SOD1 mutants cause ALS? [J].
Cleveland, DW ;
Liu, J .
NATURE MEDICINE, 2000, 6 (12) :1320-1321
[4]   Expression of human FALS SOD in motorneurons of Drosophila [J].
Elia, AJ ;
Parkes, TL ;
Kirby, K ;
St George-Hyslop, P ;
Boulianne, GL ;
Phillips, JP ;
Hilliker, AJ .
FREE RADICAL BIOLOGY AND MEDICINE, 1999, 26 (9-10) :1332-1338
[5]   Polyglutamine-mediated dysfunction and apoptotic death of a Caenorhabditis elegans sensory neuron [J].
Faber, PW ;
Alter, JR ;
MacDonald, ME ;
Hart, AC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (01) :179-184
[6]  
Fay DS, 1998, J NEUROCHEM, V71, P1616
[7]   Studying human neurodegenerative diseases in flies and worms [J].
Feany, MB .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2000, 59 (10) :847-856
[8]   A Drosophila model of Parkinson's disease [J].
Feany, MB ;
Bender, WW .
NATURE, 2000, 404 (6776) :394-398
[9]   Identification of genes that modify ataxin-1-induced neurodegeneration [J].
Fernandez-Funez, P ;
Nino-Rosales, ML ;
de Gouyon, B ;
She, WC ;
Luchak, JM ;
Martinez, P ;
Turiegano, E ;
Benito, J ;
Capovilla, M ;
Skinner, PJ ;
McCall, A ;
Canal, I ;
Orr, HT ;
Zoghbi, HY ;
Botas, J .
NATURE, 2000, 408 (6808) :101-106
[10]   Polyglutamine-expanded human huntingtin transgenes induce degeneration of Drosophila photoreceptor neurons [J].
Jackson, GR ;
Salecker, I ;
Dong, XZ ;
Yao, X ;
Arnheim, N ;
Faber, PW ;
MacDonald, ME ;
Zipursky, SL .
NEURON, 1998, 21 (03) :633-642