Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains
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...
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| Veröffentlicht in: | Neurobiology of aging 2006, Vol.27 (1), p.54-66 |
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| creator | Mishto, Michele Bellavista, Elena Santoro, Aurelia Stolzing, Alexandra Ligorio, Claudia Nacmias, Benedetta Spazzafumo, Liana Chiappelli, Martina Licastro, Federico Sorbi, Sandro Pession, Annalisa Ohm, Thomas Grune, Tilman Franceschi, Claudio |
| description | 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. |
| doi_str_mv | 10.1016/j.neurobiolaging.2004.12.004 |
| format | Article |
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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.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2004.12.004</identifier><identifier>PMID: 16298241</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Ageing ; Aging - genetics ; Aging - metabolism ; Alzheimer Disease - genetics ; Alzheimer's disease ; Biological and medical sciences ; Brain - metabolism ; Cadaver ; Cysteine Endopeptidases - genetics ; Cysteine Endopeptidases - metabolism ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Female ; Genetic Predisposition to Disease - genetics ; Humans ; Immunoproteasome ; In Vitro Techniques ; LMP2 polymorphism ; Male ; Medical sciences ; Middle Aged ; Neuroinflammation ; Neurology ; Prevalence ; Proteasome ; Proteasome Endopeptidase Complex - genetics ; Proteasome Endopeptidase Complex - metabolism ; Risk Assessment - methods ; Risk Factors</subject><ispartof>Neurobiology of aging, 2006, Vol.27 (1), p.54-66</ispartof><rights>2005 Elsevier Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-201af49567af04ab68016a00f20d489da4afc7f0a5355c1626b8b994084ed49f3</citedby><cites>FETCH-LOGICAL-c414t-201af49567af04ab68016a00f20d489da4afc7f0a5355c1626b8b994084ed49f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neurobiolaging.2004.12.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,4028,27932,27933,27934,46004</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17401213$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16298241$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mishto, Michele</creatorcontrib><creatorcontrib>Bellavista, Elena</creatorcontrib><creatorcontrib>Santoro, Aurelia</creatorcontrib><creatorcontrib>Stolzing, Alexandra</creatorcontrib><creatorcontrib>Ligorio, Claudia</creatorcontrib><creatorcontrib>Nacmias, Benedetta</creatorcontrib><creatorcontrib>Spazzafumo, Liana</creatorcontrib><creatorcontrib>Chiappelli, Martina</creatorcontrib><creatorcontrib>Licastro, Federico</creatorcontrib><creatorcontrib>Sorbi, Sandro</creatorcontrib><creatorcontrib>Pession, Annalisa</creatorcontrib><creatorcontrib>Ohm, Thomas</creatorcontrib><creatorcontrib>Grune, Tilman</creatorcontrib><creatorcontrib>Franceschi, Claudio</creatorcontrib><title>Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>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.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Ageing</subject><subject>Aging - genetics</subject><subject>Aging - metabolism</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer's disease</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Cadaver</subject><subject>Cysteine Endopeptidases - genetics</subject><subject>Cysteine Endopeptidases - metabolism</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Humans</subject><subject>Immunoproteasome</subject><subject>In Vitro Techniques</subject><subject>LMP2 polymorphism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neuroinflammation</subject><subject>Neurology</subject><subject>Prevalence</subject><subject>Proteasome</subject><subject>Proteasome Endopeptidase Complex - genetics</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>Risk Assessment - methods</subject><subject>Risk Factors</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtvEzEUhS0EoqHwF9AseKxmuHY8L4lNVVGolAoWsLbu2Nepo7Ed7AxS-fU4JFLFjtVZ-Dv28cfYGw4NB9592DWBlhQnF2fcurBtBIBsuGhKPGEr3rZDzeXYP2Ur4GNfy3aAC_Yi5x0A9LLvnrML3olxEJKv2N2t90uI-xQPhDl6qjCYanP3TVT7OD_4mPb3LvvKhQq3ZP6eXs2_78l5Su9zZVwuPaqmhC7kl-yZxTnTq3Nesh83n75ff6k3Xz_fXl9tai25PNQCOFo5tl2PFiRO3VA-hgBWgJHDaFCi1b0FbNdtq8vYbhqmcZQwSDJytOtL9u50b9n9c6F8UN5lTfOMgeKSVQ986GS7LuDHE6hTzDmRVfvkPKYHxUEddaqd-lenOupUXKgSpf76_M4yeTKP5bO_Arw9A5g1zjZh0C4_cr0ELvhxx82Jo2Lll6OksnYUNBmXSB-Uie7_Fv0BCl-bpg</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Mishto, Michele</creator><creator>Bellavista, Elena</creator><creator>Santoro, Aurelia</creator><creator>Stolzing, Alexandra</creator><creator>Ligorio, Claudia</creator><creator>Nacmias, Benedetta</creator><creator>Spazzafumo, Liana</creator><creator>Chiappelli, Martina</creator><creator>Licastro, Federico</creator><creator>Sorbi, Sandro</creator><creator>Pession, Annalisa</creator><creator>Ohm, Thomas</creator><creator>Grune, Tilman</creator><creator>Franceschi, Claudio</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>2006</creationdate><title>Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains</title><author>Mishto, Michele ; Bellavista, Elena ; Santoro, Aurelia ; Stolzing, Alexandra ; Ligorio, Claudia ; Nacmias, Benedetta ; Spazzafumo, Liana ; Chiappelli, Martina ; Licastro, Federico ; Sorbi, Sandro ; Pession, Annalisa ; Ohm, Thomas ; Grune, Tilman ; Franceschi, Claudio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-201af49567af04ab68016a00f20d489da4afc7f0a5355c1626b8b994084ed49f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Ageing</topic><topic>Aging - genetics</topic><topic>Aging - metabolism</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer's disease</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Cadaver</topic><topic>Cysteine Endopeptidases - genetics</topic><topic>Cysteine Endopeptidases - metabolism</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Humans</topic><topic>Immunoproteasome</topic><topic>In Vitro Techniques</topic><topic>LMP2 polymorphism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neuroinflammation</topic><topic>Neurology</topic><topic>Prevalence</topic><topic>Proteasome</topic><topic>Proteasome Endopeptidase Complex - genetics</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>Risk Assessment - methods</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mishto, Michele</creatorcontrib><creatorcontrib>Bellavista, Elena</creatorcontrib><creatorcontrib>Santoro, Aurelia</creatorcontrib><creatorcontrib>Stolzing, Alexandra</creatorcontrib><creatorcontrib>Ligorio, Claudia</creatorcontrib><creatorcontrib>Nacmias, Benedetta</creatorcontrib><creatorcontrib>Spazzafumo, Liana</creatorcontrib><creatorcontrib>Chiappelli, Martina</creatorcontrib><creatorcontrib>Licastro, Federico</creatorcontrib><creatorcontrib>Sorbi, Sandro</creatorcontrib><creatorcontrib>Pession, Annalisa</creatorcontrib><creatorcontrib>Ohm, Thomas</creatorcontrib><creatorcontrib>Grune, Tilman</creatorcontrib><creatorcontrib>Franceschi, Claudio</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mishto, Michele</au><au>Bellavista, Elena</au><au>Santoro, Aurelia</au><au>Stolzing, Alexandra</au><au>Ligorio, Claudia</au><au>Nacmias, Benedetta</au><au>Spazzafumo, Liana</au><au>Chiappelli, Martina</au><au>Licastro, Federico</au><au>Sorbi, Sandro</au><au>Pession, Annalisa</au><au>Ohm, Thomas</au><au>Grune, Tilman</au><au>Franceschi, Claudio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2006</date><risdate>2006</risdate><volume>27</volume><issue>1</issue><spage>54</spage><epage>66</epage><pages>54-66</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>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.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>16298241</pmid><doi>10.1016/j.neurobiolaging.2004.12.004</doi><tpages>13</tpages></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Ageing Aging - genetics Aging - metabolism Alzheimer Disease - genetics Alzheimer's disease Biological and medical sciences Brain - metabolism Cadaver Cysteine Endopeptidases - genetics Cysteine Endopeptidases - metabolism Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Genetic Predisposition to Disease - genetics Humans Immunoproteasome In Vitro Techniques LMP2 polymorphism Male Medical sciences Middle Aged Neuroinflammation Neurology Prevalence Proteasome Proteasome Endopeptidase Complex - genetics Proteasome Endopeptidase Complex - metabolism Risk Assessment - methods Risk Factors |
| title | Immunoproteasome and LMP2 polymorphism in aged and Alzheimer's disease brains |
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