14-3-3 CSF levels in sporadic Creutzfeldt–Jakob disease differ across molecular subtypes

Abstract Background The 14-3-3 protein is a physiological cellular protein expressed in various tissues, and its release to CSF reflects extensive neuronal damage as in Creutzfeldt–Jakob disease (CJD), but also in other neurological diseases. 14-3-3 protein in CSF in the proper clinical context is a...

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Veröffentlicht in:Neurobiology of aging 2009-11, Vol.30 (11), p.1842-1850
Hauptverfasser: Gmitterová, K, Heinemann, U, Bodemer, M, Krasnianski, A, Meissner, B, Kretzschmar, H.A, Zerr, I
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container_end_page 1850
container_issue 11
container_start_page 1842
container_title Neurobiology of aging
container_volume 30
creator Gmitterová, K
Heinemann, U
Bodemer, M
Krasnianski, A
Meissner, B
Kretzschmar, H.A
Zerr, I
description Abstract Background The 14-3-3 protein is a physiological cellular protein expressed in various tissues, and its release to CSF reflects extensive neuronal damage as in Creutzfeldt–Jakob disease (CJD), but also in other neurological diseases. 14-3-3 protein in CSF in the proper clinical context is a reliable diagnostic tool for sporadic CJD. However, the sensitivity varies across molecular CJD subtypes. Objective We determined the level of the 14-3-3 protein in CSF from 70 sporadic CJD patients with distinct molecular subtypes using an improved enzyme-linked immunosorbent assay (ELISA) protocol technique. Results The 14-3-3 levels varied markedly across various molecular subtypes. The most elevated levels of 14-3-3 protein were observed in the frequently occurring and classical subtypes, whereas the levels were significantly lower in the subtypes with long disease duration and atypical clinical presentation. PRNP codon 129 genotype, PrPsc isotype, disease stage and clinical subtype influenced the 14-3-3 level and the test sensitivity. Conclusions The 14-3-3 protein levels differ across molecular subtypes and might be used for their early pre-mortem identification when the codon 129 genotype is known, especially for the less common molecular subtypes such as MV2 and MM2.
doi_str_mv 10.1016/j.neurobiolaging.2008.01.007
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However, the sensitivity varies across molecular CJD subtypes. Objective We determined the level of the 14-3-3 protein in CSF from 70 sporadic CJD patients with distinct molecular subtypes using an improved enzyme-linked immunosorbent assay (ELISA) protocol technique. Results The 14-3-3 levels varied markedly across various molecular subtypes. The most elevated levels of 14-3-3 protein were observed in the frequently occurring and classical subtypes, whereas the levels were significantly lower in the subtypes with long disease duration and atypical clinical presentation. PRNP codon 129 genotype, PrPsc isotype, disease stage and clinical subtype influenced the 14-3-3 level and the test sensitivity. Conclusions The 14-3-3 protein levels differ across molecular subtypes and might be used for their early pre-mortem identification when the codon 129 genotype is known, especially for the less common molecular subtypes such as MV2 and MM2.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2008.01.007</identifier><identifier>PMID: 18328602</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>14-3-3 protein ; 14-3-3 Proteins - cerebrospinal fluid ; 14-3-3 Proteins - classification ; Aged ; Biological and medical sciences ; Creutzfeldt-Jakob Syndrome - cerebrospinal fluid ; Creutzfeldt-Jakob Syndrome - genetics ; Creutzfeldt–Jakob disease ; CSF ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dementia ; Development. Senescence. Regeneration. Transplantation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Fundamental and applied biological sciences. Psychology ; Genotype ; Humans ; Internal Medicine ; Male ; Medical sciences ; Middle Aged ; Neurology ; Prion Proteins ; Prions - genetics ; PrPSc Proteins - genetics ; PrPSc Proteins - metabolism ; Retrospective Studies ; Statistics, Nonparametric ; Vertebrates: nervous system and sense organs</subject><ispartof>Neurobiology of aging, 2009-11, Vol.30 (11), p.1842-1850</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-caf12d567aaca6ad81f7fcbdb57b8962b8bf843d7cfaddd90c2605ac50b5193b3</citedby><cites>FETCH-LOGICAL-c501t-caf12d567aaca6ad81f7fcbdb57b8962b8bf843d7cfaddd90c2605ac50b5193b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197458008000250$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=23922637$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18328602$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gmitterová, K</creatorcontrib><creatorcontrib>Heinemann, U</creatorcontrib><creatorcontrib>Bodemer, M</creatorcontrib><creatorcontrib>Krasnianski, A</creatorcontrib><creatorcontrib>Meissner, B</creatorcontrib><creatorcontrib>Kretzschmar, H.A</creatorcontrib><creatorcontrib>Zerr, I</creatorcontrib><title>14-3-3 CSF levels in sporadic Creutzfeldt–Jakob disease differ across molecular subtypes</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract Background The 14-3-3 protein is a physiological cellular protein expressed in various tissues, and its release to CSF reflects extensive neuronal damage as in Creutzfeldt–Jakob disease (CJD), but also in other neurological diseases. 14-3-3 protein in CSF in the proper clinical context is a reliable diagnostic tool for sporadic CJD. However, the sensitivity varies across molecular CJD subtypes. Objective We determined the level of the 14-3-3 protein in CSF from 70 sporadic CJD patients with distinct molecular subtypes using an improved enzyme-linked immunosorbent assay (ELISA) protocol technique. Results The 14-3-3 levels varied markedly across various molecular subtypes. The most elevated levels of 14-3-3 protein were observed in the frequently occurring and classical subtypes, whereas the levels were significantly lower in the subtypes with long disease duration and atypical clinical presentation. PRNP codon 129 genotype, PrPsc isotype, disease stage and clinical subtype influenced the 14-3-3 level and the test sensitivity. Conclusions The 14-3-3 protein levels differ across molecular subtypes and might be used for their early pre-mortem identification when the codon 129 genotype is known, especially for the less common molecular subtypes such as MV2 and MM2.</description><subject>14-3-3 protein</subject><subject>14-3-3 Proteins - cerebrospinal fluid</subject><subject>14-3-3 Proteins - classification</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Creutzfeldt-Jakob Syndrome - cerebrospinal fluid</subject><subject>Creutzfeldt-Jakob Syndrome - genetics</subject><subject>Creutzfeldt–Jakob disease</subject><subject>CSF</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dementia</subject><subject>Development. Senescence. Regeneration. Transplantation</subject><subject>Disease Progression</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genotype</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Prion Proteins</subject><subject>Prions - genetics</subject><subject>PrPSc Proteins - genetics</subject><subject>PrPSc Proteins - metabolism</subject><subject>Retrospective Studies</subject><subject>Statistics, Nonparametric</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNksuKFDEUhgtRnHb0FaQWXlZVniSVShWIII3thQEXoxs3IZeTIT3pqjapGmhXvoNv6JOYshtFFyIEzub7_5Nz_lMUjwjUBEj7bFsPOMdR-zGoKz9c1RSgq4HUAOJWsSKcdxVpenG7WAHpRdXwDs6KeyltIRONaO8WZ6RjtGuBropPpKlYxcr15aYMeIMhlX4o036MynpTriPO0xeHwU7fv357p65HXVqfUCXM1TmMpTJxTKncjQHNHFQs06ynwx7T_eKOUyHhg1M9Lz5uXn1Yv6ku3r9-u355URkOZKqMcoRa3gqljGqV7YgTzmirudBd31Ldadc1zArjlLW2B0Nb4CqLNSc90-y8eHr03cfx84xpkjufDIagBhznJAVrgBMm2kw--SdJCXQN71kGnx_Bn7NFdHIf_U7FgyQglxTkVv6ZglxSkEBk3nGWPzz1mfUO7W_xae0ZeHwCVDIquKgG49MvjrKe0pYtRpsjl3PBG49RJuNxMGh9RDNJO_r__dGLv4xM8IPPva_xgGk7znHIGUkiE5UgL5fLWQ4H8gPKgf0ApkHEww</recordid><startdate>20091101</startdate><enddate>20091101</enddate><creator>Gmitterová, K</creator><creator>Heinemann, U</creator><creator>Bodemer, M</creator><creator>Krasnianski, A</creator><creator>Meissner, B</creator><creator>Kretzschmar, H.A</creator><creator>Zerr, I</creator><general>Elsevier Inc</general><general>Elsevier</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>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20091101</creationdate><title>14-3-3 CSF levels in sporadic Creutzfeldt–Jakob disease differ across molecular subtypes</title><author>Gmitterová, K ; Heinemann, U ; Bodemer, M ; Krasnianski, A ; Meissner, B ; Kretzschmar, H.A ; Zerr, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-caf12d567aaca6ad81f7fcbdb57b8962b8bf843d7cfaddd90c2605ac50b5193b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>14-3-3 protein</topic><topic>14-3-3 Proteins - cerebrospinal fluid</topic><topic>14-3-3 Proteins - classification</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Creutzfeldt-Jakob Syndrome - cerebrospinal fluid</topic><topic>Creutzfeldt-Jakob Syndrome - genetics</topic><topic>Creutzfeldt–Jakob disease</topic><topic>CSF</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dementia</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>Disease Progression</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genotype</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Prion Proteins</topic><topic>Prions - genetics</topic><topic>PrPSc Proteins - genetics</topic><topic>PrPSc Proteins - metabolism</topic><topic>Retrospective Studies</topic><topic>Statistics, Nonparametric</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gmitterová, K</creatorcontrib><creatorcontrib>Heinemann, U</creatorcontrib><creatorcontrib>Bodemer, M</creatorcontrib><creatorcontrib>Krasnianski, A</creatorcontrib><creatorcontrib>Meissner, B</creatorcontrib><creatorcontrib>Kretzschmar, H.A</creatorcontrib><creatorcontrib>Zerr, I</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>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gmitterová, K</au><au>Heinemann, U</au><au>Bodemer, M</au><au>Krasnianski, A</au><au>Meissner, B</au><au>Kretzschmar, H.A</au><au>Zerr, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>14-3-3 CSF levels in sporadic Creutzfeldt–Jakob disease differ across molecular subtypes</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2009-11-01</date><risdate>2009</risdate><volume>30</volume><issue>11</issue><spage>1842</spage><epage>1850</epage><pages>1842-1850</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>Abstract Background The 14-3-3 protein is a physiological cellular protein expressed in various tissues, and its release to CSF reflects extensive neuronal damage as in Creutzfeldt–Jakob disease (CJD), but also in other neurological diseases. 14-3-3 protein in CSF in the proper clinical context is a reliable diagnostic tool for sporadic CJD. However, the sensitivity varies across molecular CJD subtypes. Objective We determined the level of the 14-3-3 protein in CSF from 70 sporadic CJD patients with distinct molecular subtypes using an improved enzyme-linked immunosorbent assay (ELISA) protocol technique. Results The 14-3-3 levels varied markedly across various molecular subtypes. The most elevated levels of 14-3-3 protein were observed in the frequently occurring and classical subtypes, whereas the levels were significantly lower in the subtypes with long disease duration and atypical clinical presentation. PRNP codon 129 genotype, PrPsc isotype, disease stage and clinical subtype influenced the 14-3-3 level and the test sensitivity. Conclusions The 14-3-3 protein levels differ across molecular subtypes and might be used for their early pre-mortem identification when the codon 129 genotype is known, especially for the less common molecular subtypes such as MV2 and MM2.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>18328602</pmid><doi>10.1016/j.neurobiolaging.2008.01.007</doi><tpages>9</tpages></addata></record>
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subjects 14-3-3 protein
14-3-3 Proteins - cerebrospinal fluid
14-3-3 Proteins - classification
Aged
Biological and medical sciences
Creutzfeldt-Jakob Syndrome - cerebrospinal fluid
Creutzfeldt-Jakob Syndrome - genetics
Creutzfeldt–Jakob disease
CSF
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Dementia
Development. Senescence. Regeneration. Transplantation
Disease Progression
Enzyme-Linked Immunosorbent Assay
Female
Fundamental and applied biological sciences. Psychology
Genotype
Humans
Internal Medicine
Male
Medical sciences
Middle Aged
Neurology
Prion Proteins
Prions - genetics
PrPSc Proteins - genetics
PrPSc Proteins - metabolism
Retrospective Studies
Statistics, Nonparametric
Vertebrates: nervous system and sense organs
title 14-3-3 CSF levels in sporadic Creutzfeldt–Jakob disease differ across molecular subtypes
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