Brain proteasomal function in sporadic Parkinson's disease and related disorders

被引:68
作者
Furukawa, Y
Vigouroux, S
Wong, H
Guttman, M
Rajput, AH
Ang, L
Briand, M
Kish, SJ
Briand, Y
机构
[1] Univ Toronto, Movement Dis Res Lab R211, Ctr Addict & Mental Hlth, Clarke Div, Toronto, ON M5T 1R8, Canada
[2] Univ Clermont Ferrand, Lab Biochem Appl, Clermont Ferrand, France
[3] Univ Toronto, Human Neurochem Pathol Lab, Ctr Addict & Mental Hlth, Clarke Div, Toronto, ON M5T 1R8, Canada
[4] Univ Saskatchewan, Div Neurol, Saskatoon, SK, Canada
[5] Univ Western Ontario, Dept Pathol, London, ON, Canada
关键词
D O I
10.1002/ana.10207
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal. function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.
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页码:779 / 782
页数:4
相关论文
共 20 条
[1]   α-Synuclein and the Parkinson's disease-related mutant Ala53Thr-α-synuclein do not undergo proteasomal degradation in HEK293 and neuronal cells [J].
Ancolio, K ;
da Costa, CA ;
Uéda, K ;
Checler, F .
NEUROSCIENCE LETTERS, 2000, 285 (02) :79-82
[2]   Impairment of the ubiquitin-proteasome system by protein aggregation [J].
Bence, NF ;
Sampat, RM ;
Kopito, RR .
SCIENCE, 2001, 292 (5521) :1552-1555
[3]   Degradation of α-synuclein by proteasome [J].
Bennett, MC ;
Bishop, JF ;
Leng, Y ;
Chock, PB ;
Chase, TN ;
Mouradian, MM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (48) :33855-33858
[4]   Degradation of oxidized proteins by the 20S proteasome [J].
Davies, KJA .
BIOCHIMIE, 2001, 83 (3-4) :301-310
[5]   Widespread alterations of α-synuclein in multiple system atrophy [J].
Dickson, DW ;
Liu, WK ;
Hardy, J ;
Farrer, M ;
Mehta, N ;
Uitti, R ;
Mark, M ;
Zimmerman, T ;
Golbe, L ;
Sage, J ;
Sima, A ;
D'Amato, C ;
Albin, R ;
Gilman, S ;
Yen, SH .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (04) :1241-1251
[6]   Proteasomes and proteasome inhibition in the central nervous system [J].
Ding, QX ;
Keller, JN .
FREE RADICAL BIOLOGY AND MEDICINE, 2001, 31 (05) :574-584
[7]   Distribution of proteasomes and of the five proteolytic activities in rat tissues [J].
Farout, L ;
Lamare, MC ;
Cardozo, C ;
Harrisson, M ;
Briand, Y ;
Briand, M .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2000, 374 (02) :207-212
[8]   Rat α-synuclein interacts with Tat binding protein 1, a component of the 26S proteasomal complex [J].
Ghee, M ;
Fournier, A ;
Mallet, J .
JOURNAL OF NEUROCHEMISTRY, 2000, 75 (05) :2221-2224
[9]   Consensus statement on the diagnosis of multiple system atrophy [J].
Gilman, S ;
Low, PA ;
Quinn, N ;
Albanese, A ;
Ben-Shlomo, Y ;
Fowler, CJ ;
Kaufman, H ;
Klockgether, T ;
Lang, AE ;
Lantos, PL ;
Litvan, I ;
Mathias, CJ ;
Oliver, E ;
Robertson, D ;
Schatz, I ;
Wenning, GK .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1999, 163 (01) :94-98
[10]   Dopamine induces proteasome inhibition in neural PC12 cell line [J].
Keller, JN ;
Huang, FF ;
Dimayuga, ER ;
Maragos, WF .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (10) :1037-1042