Proteasome inhibition and Parkinson's disease modeling

Jordi Bové, Chun Zhou, Vernice Jackson-Lewis, Julie Taylor, Yaping Chu, Hardy J. Rideout, Du Chu Wu, Jeffrey H. Kordower, Leonard Petrucelli, Serge Przedborski

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

Impaired proteasome function is a potential mechanism for dopaminergic neuron degeneration. To model this molecular defect, we administered systemically the reversible lipophilic proteasome inhibitor, carbobenzoxy-L-isoleucyl-γ-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents. In contrast to a previous report, this approach failed to cause any detectable behavioral or neuropathological abnormality in either rats or mice. Although theoretically appealing, this specific model of Parkinson's disease appears to exhibit poor reproducibility.

Original languageEnglish (US)
Pages (from-to)260-264
Number of pages5
JournalAnnals of Neurology
Volume60
Issue number2
DOIs
StatePublished - Aug 2006

Fingerprint

Nerve Degeneration
Proteasome Inhibitors
Molecular Models
Dopaminergic Neurons
Proteasome Endopeptidase Complex
Parkinson Disease
Rodentia
leucinal

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Bové, J., Zhou, C., Jackson-Lewis, V., Taylor, J., Chu, Y., Rideout, H. J., ... Przedborski, S. (2006). Proteasome inhibition and Parkinson's disease modeling. Annals of Neurology, 60(2), 260-264. https://doi.org/10.1002/ana.20937

Proteasome inhibition and Parkinson's disease modeling. / Bové, Jordi; Zhou, Chun; Jackson-Lewis, Vernice; Taylor, Julie; Chu, Yaping; Rideout, Hardy J.; Wu, Du Chu; Kordower, Jeffrey H.; Petrucelli, Leonard; Przedborski, Serge.

In: Annals of Neurology, Vol. 60, No. 2, 08.2006, p. 260-264.

Research output: Contribution to journalArticle

Bové, J, Zhou, C, Jackson-Lewis, V, Taylor, J, Chu, Y, Rideout, HJ, Wu, DC, Kordower, JH, Petrucelli, L & Przedborski, S 2006, 'Proteasome inhibition and Parkinson's disease modeling', Annals of Neurology, vol. 60, no. 2, pp. 260-264. https://doi.org/10.1002/ana.20937
Bové J, Zhou C, Jackson-Lewis V, Taylor J, Chu Y, Rideout HJ et al. Proteasome inhibition and Parkinson's disease modeling. Annals of Neurology. 2006 Aug;60(2):260-264. https://doi.org/10.1002/ana.20937
Bové, Jordi ; Zhou, Chun ; Jackson-Lewis, Vernice ; Taylor, Julie ; Chu, Yaping ; Rideout, Hardy J. ; Wu, Du Chu ; Kordower, Jeffrey H. ; Petrucelli, Leonard ; Przedborski, Serge. / Proteasome inhibition and Parkinson's disease modeling. In: Annals of Neurology. 2006 ; Vol. 60, No. 2. pp. 260-264.
@article{d9cb51257a024a46944ade568460a795,
title = "Proteasome inhibition and Parkinson's disease modeling",
abstract = "Impaired proteasome function is a potential mechanism for dopaminergic neuron degeneration. To model this molecular defect, we administered systemically the reversible lipophilic proteasome inhibitor, carbobenzoxy-L-isoleucyl-γ-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents. In contrast to a previous report, this approach failed to cause any detectable behavioral or neuropathological abnormality in either rats or mice. Although theoretically appealing, this specific model of Parkinson's disease appears to exhibit poor reproducibility.",
author = "Jordi Bov{\'e} and Chun Zhou and Vernice Jackson-Lewis and Julie Taylor and Yaping Chu and Rideout, {Hardy J.} and Wu, {Du Chu} and Kordower, {Jeffrey H.} and Leonard Petrucelli and Serge Przedborski",
year = "2006",
month = "8",
doi = "10.1002/ana.20937",
language = "English (US)",
volume = "60",
pages = "260--264",
journal = "Annals of Neurology",
issn = "0364-5134",
publisher = "John Wiley and Sons Inc.",
number = "2",

}

TY - JOUR

T1 - Proteasome inhibition and Parkinson's disease modeling

AU - Bové, Jordi

AU - Zhou, Chun

AU - Jackson-Lewis, Vernice

AU - Taylor, Julie

AU - Chu, Yaping

AU - Rideout, Hardy J.

AU - Wu, Du Chu

AU - Kordower, Jeffrey H.

AU - Petrucelli, Leonard

AU - Przedborski, Serge

PY - 2006/8

Y1 - 2006/8

N2 - Impaired proteasome function is a potential mechanism for dopaminergic neuron degeneration. To model this molecular defect, we administered systemically the reversible lipophilic proteasome inhibitor, carbobenzoxy-L-isoleucyl-γ-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents. In contrast to a previous report, this approach failed to cause any detectable behavioral or neuropathological abnormality in either rats or mice. Although theoretically appealing, this specific model of Parkinson's disease appears to exhibit poor reproducibility.

AB - Impaired proteasome function is a potential mechanism for dopaminergic neuron degeneration. To model this molecular defect, we administered systemically the reversible lipophilic proteasome inhibitor, carbobenzoxy-L-isoleucyl-γ-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents. In contrast to a previous report, this approach failed to cause any detectable behavioral or neuropathological abnormality in either rats or mice. Although theoretically appealing, this specific model of Parkinson's disease appears to exhibit poor reproducibility.

UR - http://www.scopus.com/inward/record.url?scp=33746850545&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746850545&partnerID=8YFLogxK

U2 - 10.1002/ana.20937

DO - 10.1002/ana.20937

M3 - Article

C2 - 16862585

AN - SCOPUS:33746850545

VL - 60

SP - 260

EP - 264

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

IS - 2

ER -