Pathogenic effects of α-synuclein aggregation

被引：74

作者：

Lundvig, D ^{[1
]}

Lindersson, E ^{[1
]}

Jensen, PH ^{[1
]}

机构：

[1] Aarhus Univ, Dept Med Biochem, DK-8000 Aarhus, Denmark

来源：

MOLECULAR BRAIN RESEARCH | 2005年 / 134卷 / 01期

关键词：

Parkinson disease; Lewy body dementia; multiple systems atrophy; Lewy body; protein aggregation; filaments; amyloid; oligomers; synuclein; neurodegeneration;

D O I：

10.1016/j.molbrainres.2004.09.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Biochemical and genetic evidence point towards alpha-synuclein aggregation as having a pivotal role in the onset and progression of several neurodegenerative disorders, including Parkinson's disease, multiple system atrophy and Lewy body dementia. We review recent data on how alpha-synuclein aggregates may impact on cellular homeostatic mechanisms including cellular transport and degradation and transcriptional regulation. alpha-Synuclein aggregates can exist as several molecular species and their different features are discussed in the context of the methodologies used for their study and the many chemical and physical factors that influence their formation. (C) 2004 Elsevier B.V. All rights reserved.

引用

页码：3 / 17

页数：15

共 127 条

[1] Mice lacking α-synuclein display functional deficits in the nigrostriatal dopamine system [J].

Abeliovich, A ;

Schmitz, Y ;

Fariñas, I ;

Choi-Lundberg, D ;

Ho, WH ;

Castillo, PE ;

Shinsky, N ;

Verdugo, JMG ;

Armanini, M ;

Ryan, A ;

Hynes, M ;

Phillips, H ;

Sulzer, D ;

Rosenthal, A .

NEURON, 2000, 25 (01) :239-252

[2] HMGB proteins and gene expression [J].

Agresti, A ;

Bianchi, ME .

CURRENT OPINION IN GENETICS & DEVELOPMENT, 2003, 13 (02) :170-178

[3] Tubulin seeds α-synuclein fibril formation [J].

Alim, MA ;

Hossain, MS ;

Arima, K ;

Takeda, K ;

Izumiyama, Y ;

Nakamura, M ;

Kaji, H ;

Shinoda, T ;

Hisanaga, S ;

Uéda, K .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (03) :2112-2117

[4] Lewy body in neurodegeneration with brain iron accumulation type 1 is immunoreactive for α-synuclein [J].

Arawaka, S ;

Saito, Y ;

Murayama, S ;

Mori, H .

NEUROLOGY, 1998, 51 (03) :887-889

[5] Cellular co-localization of phosphorylated tau- and NACP/α-synuclein-epitopes in Lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies [J].

Arima, K ;

Hirai, S ;

Sunohara, N ;

Aoto, K ;

Izumiyama, Y ;

Uéda, K ;

Ikeda, K ;

Kawai, M .

BRAIN RESEARCH, 1999, 843 (1-2) :53-61

[6] NACP/α-synuclein immunoreactivity in fibrillary components of neuronal and oligodendroglial cytoplasmic inclusions in the pontine nuclei in multiple system atrophy [J].

Arima, K ;

Uéda, K ;

Sunohara, N ;

Arakawa, K ;

Hirai, S ;

Nakamura, M ;

Tonozuka-Uehara, H ;

Kawai, M .

ACTA NEUROPATHOLOGICA, 1998, 96 (05) :439-444

[7] Immunoelectron-microscopic demonstration of NACP/α-synuclein-epitopes on the filamentous component of Lewy bodies in Parkinson's disease and in dementia with Lewy bodies [J].

Arima, K ;

Uéda, K ;

Sunohara, N ;

Hirai, S ;

Izumiyama, Y ;

Tonozuka-Uehara, H ;

Kawai, M .

BRAIN RESEARCH, 1998, 808 (01) :93-100

[8] 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

[9]

Baba M, 1998, AM J PATHOL, V152, P879

[10] Molecular chaperones enhance the degradation of expanded polyglutamine repeat androgen receptor in a cellular model of spinal and bulbar muscular atrophy [J].

Bailey, CK ;

Andriola, IFM ;

Kampinga, HH ;

Merry, DE .

HUMAN MOLECULAR GENETICS, 2002, 11 (05) :515-523

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