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Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains
journal contributionposted on 2015-03-05, 14:30 authored by Michele Mishto, Elena Bellavista, Aurelia Santoro, Alexandra StolzingAlexandra 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.
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”
- Mechanical, Electrical and Manufacturing Engineering
Published inNeurobiology of Aging
Pages54 - 66
CitationMISHTO, 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
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NotesThis article is closed access.