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Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains

journal contribution
posted on 05.03.2015 by Michele Mishto, Elena Bellavista, Aurelia Santoro, Alexandra Stolzing, Claudia Ligorio, Benedetta Nacmias, Liana Spazzafumo, Martina Chiappelli, Federico Licastro, Sandro Sorbi, Annalisa Pession, Thomas Ohm, Tilman Grune, Claudio Franceschi
In this study, we investigated the presence and role of immunoproteasome and its LMP2 subunit polymorphism at codon 60 in Alzheimer's disease (AD). Immunoproteasome was present in brain areas such as hippocampus and cerebellum and localized in neurons, astrocytes and endothelial cells. A higher expression of immunoproteasome was found in brain of AD patients than in brain of non-demented elderly, being its expression in young brain negligible or absent. Furthermore, AD affected regions showed a partial decrease in proteasome trypsin-like activity. The study of LMP2 polymorphism (R/H) showed that it does not influence LMP2 expression (neither the mRNA nor mature protein) in brain tissue. However, control brain areas of AD patients carrying the RR genotype showed an increased proteasome activity in comparison with RH carriers. To test whether this effect of the genotype might be related to AD onset we performed a genetic study, which allowed us to exclude an association of LMP2 codon 60 polymorphism with AD onset, despite its influence on the proteasome activity in human brain. © 2005 Elsevier Inc. All rights reserved.

Funding

This work was financed in part by a grant from project PROTAGE and FUNCTIONAGE, sponsored by the European Commission fifth Framework Program “Aging of the Population”

History

School

  • Mechanical, Electrical and Manufacturing Engineering

Published in

Neurobiology of Aging

Volume

27

Issue

1

Pages

54 - 66

Citation

MISHTO, M. ... et al, 2006. Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains. Neurobiology of Aging, 27 (1), pp. 54 - 66.

Publisher

© Elsevier Inc

Version

VoR (Version of Record)

Publisher statement

This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/

Publication date

2006

Notes

This article is closed access.

ISSN

0197-4580

Language

en

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