Mechanism of neurodegenerative disease: role of the ubiquitin proteasome system

Annals of Medicine
Leonardo Petrucelli, Ted M Dawson

Abstract

Many neurodegenerative disorders such as Alzheimer's disease (AD) Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) are characterized by neuronal damage that may be caused by toxic, abnormal, aggregation-prone proteins. The purpose of this review is threefold: 1) to provide the reader with an overview of the genes involved in the abnormal processing and accumulation of misfolded proteins in neurodegenerative diseases using PD as a model disease; 2) to understand the cellular mechanisms for disposal of abnormal proteins, and the effects of toxic protein accumulation on ubiquitin proteasome system (UPS) and neuronal survival and 3) to discuss the development and challenges of cell culture and animal models for a rational and effective treatment for these disorders.

References

Oct 7, 1994·Cell·A Ciechanover
Apr 4, 1997·The Journal of Biological Chemistry·B BercovichA Ciechanover
Jul 12, 1997·Lancet·R W Carrell, D A Lomas
Oct 17, 1998·Nature·E LeroyM H Polymeropoulos
Nov 24, 1999·The Journal of Biological Chemistry·M C BennettM M Mouradian
Apr 4, 2000·Nature·M B Feany, W W Bender
Nov 15, 2000·Proceedings of the National Academy of Sciences of the United States of America·Y ZhangT M Dawson
Jan 4, 2001·Neuroscience Letters·K S McNaught, P Jenner
Jun 8, 2001·Movement Disorders : Official Journal of the Movement Disorder Society·L I GolbeJ I Sage
Sep 18, 2001·Annals of Neurology·M FarrerJ W Langston
Nov 15, 2001·Annals of Neurology·D M MaraganoreW A Rocca
Nov 17, 2001·JAMA : the Journal of the American Medical Association·E R MartinJ M Vance
Jun 19, 2002·Acta Neuropathologica·John E DudaJohn Q Trojanowski
Oct 11, 2002·Human Molecular Genetics·Lisette G G C VerhoefNico P Dantuma
Jan 29, 2003·The Journal of Biological Chemistry·Heather SnyderBenjamin Wolozin
Jul 23, 2003·Nature Biotechnology·Kristina LindstenNico P Dantuma

❮ Previous
Next ❯

Citations

Apr 17, 2009·Cellular and Molecular Neurobiology·Takuya OshikawaTsutomu Araki
Feb 23, 2008·Proceedings of the National Academy of Sciences of the United States of America·Chad A DickeyLeonard Petrucelli
Mar 29, 2011·Cold Spring Harbor Perspectives in Biology·Steven Finkbeiner
Feb 17, 2007·The Journal of Clinical Investigation·Chad A DickeyLeonard Petrucelli
Sep 25, 2012·Molecular Neurodegeneration·Keiichi InoueAsa Abeliovich
Mar 13, 2012·International Journal of Environmental Research and Public Health·Syed F AliSyed Z Imam
Mar 16, 2007·Proceedings of the National Academy of Sciences of the United States of America·Christian ZuberJürgen Roth
Jul 18, 2009·Journal of Neuroscience Research·Kenneth M RosenHenry W Querfurth
Jun 16, 2011·Neurochemistry International·Kangyong LiuXiaojiang Sun
Mar 10, 2010·Neurobiology of Disease·Johanna KnöferlePaul Lingor
Feb 17, 2009·Neurobiology of Aging·Sara RollinsonStuart M Pickering-Brown
May 28, 2016·Annals of Clinical and Translational Neurology·Barış GençP Hande Özdinler
Sep 22, 2012·Journal of Neurochemistry·Jörg HanriederJonas Bergquist
Jul 24, 2010·Journal of Neurochemistry·Wenjie XieWeidong Le
Feb 16, 2006·Journal of Molecular Biology·Angela D WilliamsRonald Wetzel
Dec 3, 2005·Journal of Molecular Biology·Anusri BhattacharyyaRonald Wetzel
Apr 5, 2011·Molecular and Cellular Neurosciences·Michele NutiniPatrizia Longone
Jun 4, 2010·Expert Review of Neurotherapeutics·W Michael CaudleJing Zhang
Jan 19, 2007·Biochimica Et Biophysica Acta·Lloyd A GreeneSubhas C Biswas
Dec 18, 2013·Molecular Neurodegeneration·Rodrigo A QuintanillaGail V W Johnson

❮ Previous
Next ❯

Related Concepts

Related Feeds

Amyloid Lateral Sclerosis

Amyotrophic Lateral Sclerosis (ALS) is a progressive nervous system disease associated with the death of neurons that control voluntary muscles. Discover the latest research on ALS here.

Related Papers

Nature Reviews. Neuroscience
Paul J Muchowski, Jennifer L Wacker
Sheng li ke xue jin zhan [Progress in physiology]
Wen-Wei LiHui-Min Ren
© 2022 Meta ULC. All rights reserved