The role of the ubiquitin proteasome system in Alzheimer's disease.

Détails

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_8D985D4B3A96
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
The role of the ubiquitin proteasome system in Alzheimer's disease.
Périodique
Experimental Biology and Medicine
Auteur(s)
Riederer B.M., Leuba G., Vernay A., Riederer I.M.
ISSN
1535-3699 (Electronic)
ISSN-L
1535-3699
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
236
Numéro
3
Pages
268-276
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
Today, Alzheimer's disease (AD) is one of the most important age-related neurodegenerative diseases, but its etiology remains still unknown. Since the discovery that the hallmark structures of this disease i.e. the formation of amyloid fibers could be the product of ubiquitin-mediated protein degradation defects, it has become clear that the ubiquitin-proteasome system (UPS), usually essential for protein repair, turnover and degradation, is perturbed in this disease. Different aspects of normal and pathological aging are discussed with respect to protein repair and degradation via the UPS, as well as consequences of a deficit in the UPS in AD. Selective protein oxidation may cause protein damage, or protein mutations may induce a dysfunction of the proteasome. Such events eventually lead to activation of cell death pathways and to an aberrant aggregation or incorporation of ubiquitinated proteins into hallmark structures. Aggresome formation is also observed in other neurodegenerative diseases, suggesting that an activation of similar mechanisms must occur in neurodegeneration as a basic phenomenon. It is essential to discuss therapeutic ways to investigate the UPS dysfunction in the human brain and to identify specific targets to hold or stop cell decay.
Pubmed
Web of science
Création de la notice
28/03/2011 11:02
Dernière modification de la notice
03/03/2018 19:16
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