CSF Amyloid-beta 38 as a novel diagnostic marker for dementia with Lewy bodies
Identifieur interne : 000146 ( Hal/Corpus ); précédent : 000145; suivant : 000147CSF Amyloid-beta 38 as a novel diagnostic marker for dementia with Lewy bodies
Auteurs : Ezra Mulugeta ; Elisabet Londos ; Clive Ballard ; Guido Alves ; Henrik Zetterberg ; Kaj Blennow ; Ragnhild Skogseth ; Lennart Minthon ; Dag AarslandSource :
- Journal of Neurology, Neurosurgery and Psychiatry [ 0022-3050 ] ; 2010-11-03.
English descriptors
Abstract
Background The clinical distinction between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is sometimes difficult, particularly in mild cases. Although cerebrospinal fluid (CSF) markers such as Aβ42 and P-tau can distinguish between AD and normal controls, their ability to distinguish between AD and DLB is not adequate. Objective This study aims at investigating whether CSF markers, in particular the level of Aβ38, can differentiate between mild AD and DLB. Methods In total 85 individuals were included after standardized diagnostic procedures: 30 diagnosed as probable AD, 23 probable DLB, 20 with probable Parkinson's disease dementia (PDD), and 12 non-demented controls subjects. CSF levels of Aβ38, Aβ40 and Aβ42 were determined using commercially available Ultra-Sensitive multi-array kit assay (MSD) for human Aβ peptides. Total-tau (T-tau) and Phosphorylated tau (P-Tau) were analysed using ELISA (Innotest). In addition, combinations (Aβ42/Aβ38, Aβ42/Aβ40, Aβ42/P-tau, and Aβ42/Aβ38/P-tau) were assessed. Results Significant between-group differences were found for all CSF measures, and all except Aβ40, Aβ42, and Aβ42/P-tau differed between AD and DLB. Aβ42/Aβ38 ratio was the measure that best discriminated between AD and DLB (AUC 0.781; p<0.005), with sensitivity 74% and specificity 77%. Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy. Studies with independent and larger samples and a priori cut-offs are needed to test this hypothesis.
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DOI: 10.1136/jnnp.2009.199398
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status="VALID"> <orgName>University of Bergen</orgName> <desc> <address> <country key="NO"></country> </address> </desc></org></tutelle></tutelles></hal:affiliation></affiliation></author><author><name sortKey="Minthon, Lennart" sort="Minthon, Lennart" uniqKey="Minthon L" first="Lennart" last="Minthon">Lennart Minthon</name><affiliation><hal:affiliation type="laboratory" xml:id="struct-154501" status="INCOMING"> <orgName>University of Lund</orgName> <desc> <address> <country key="NO"></country> </address> </desc> <listRelation> <relation active="#struct-304690" type="direct"></relation> </listRelation><tutelles><tutelle active="#struct-304690" type="direct"><org type="institution" xml:id="struct-304690" status="INCOMING"> <orgName>University of Lund</orgName> <desc> <address> <country key="FR"></country> </address> </desc></org></tutelle></tutelles></hal:affiliation></affiliation></author><author><name sortKey="Aarsland, Dag" sort="Aarsland, Dag" uniqKey="Aarsland D" first="Dag" last="Aarsland">Dag Aarsland</name><affiliation><hal:affiliation type="laboratory" xml:id="struct-154505" status="INCOMING"> <orgName>Stavanger University Hospital</orgName> <desc> <address> <country key="GB"></country> </address> </desc> <listRelation> <relation active="#struct-338946" type="direct"></relation> </listRelation><tutelles><tutelle active="#struct-338946" type="direct"><org type="institution" xml:id="struct-338946" status="INCOMING"> <orgName>Stavanger University Hospital</orgName> <desc> <address> <country key="FR"></country> </address> </desc></org></tutelle></tutelles></hal:affiliation></affiliation></author></analytic><idno type="DOI">10.1136/jnnp.2009.199398</idno><series><title level="j">Journal of Neurology, Neurosurgery and Psychiatry</title><idno type="ISSN">0022-3050</idno><imprint><date type="datePub">2010-11-03</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>ALZHEIMER'S DISEASE</term><term>DEMENTIA</term><term>LEWY BODY</term><term>PARKINSON'S DISEASE</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background The clinical distinction between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is sometimes difficult, particularly in mild cases. Although cerebrospinal fluid (CSF) markers such as Aβ42 and P-tau can distinguish between AD and normal controls, their ability to distinguish between AD and DLB is not adequate. Objective This study aims at investigating whether CSF markers, in particular the level of Aβ38, can differentiate between mild AD and DLB. Methods In total 85 individuals were included after standardized diagnostic procedures: 30 diagnosed as probable AD, 23 probable DLB, 20 with probable Parkinson's disease dementia (PDD), and 12 non-demented controls subjects. CSF levels of Aβ38, Aβ40 and Aβ42 were determined using commercially available Ultra-Sensitive multi-array kit assay (MSD) for human Aβ peptides. Total-tau (T-tau) and Phosphorylated tau (P-Tau) were analysed using ELISA (Innotest). In addition, combinations (Aβ42/Aβ38, Aβ42/Aβ40, Aβ42/P-tau, and Aβ42/Aβ38/P-tau) were assessed. Results Significant between-group differences were found for all CSF measures, and all except Aβ40, Aβ42, and Aβ42/P-tau differed between AD and DLB. Aβ42/Aβ38 ratio was the measure that best discriminated between AD and DLB (AUC 0.781; p<0.005), with sensitivity 74% and specificity 77%. Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy. Studies with independent and larger samples and a priori cut-offs are needed to test this hypothesis.</div></front></TEI><hal api="V3"> <titleStmt> <title xml:lang="en">CSF Amyloid-beta 38 as a novel diagnostic marker for dementia with Lewy bodies</title> <author role="aut"> <persName> <forename type="first">Ezra</forename> <surname>Mulugeta</surname> </persName> <idno type="halauthorid">604715</idno> <affiliation ref="#struct-154500"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Elisabet</forename> <surname>Londos</surname> </persName> <idno type="halauthorid">604716</idno> <affiliation ref="#struct-154501"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Clive</forename> <surname>Ballard</surname> </persName> <idno type="halauthorid">604717</idno> <affiliation ref="#struct-132603"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Guido</forename> <surname>Alves</surname> </persName> <idno 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n="PEER">PEER Publishing and the Ecology of European Research</idno> </seriesStmt> <notesStmt> <note type="audience" n="2">International</note> <note type="popular" n="0">No</note> <note type="peer" n="1">Yes</note> </notesStmt> <sourceDesc> <biblStruct> <analytic> <title xml:lang="en">CSF Amyloid-beta 38 as a novel diagnostic marker for dementia with Lewy bodies</title> <author role="aut"> <persName> <forename type="first">Ezra</forename> <surname>Mulugeta</surname> </persName> <idno type="halauthorid">604715</idno> <affiliation ref="#struct-154500"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Elisabet</forename> <surname>Londos</surname> </persName> <idno type="halauthorid">604716</idno> <affiliation ref="#struct-154501"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Clive</forename> <surname>Ballard</surname> </persName> <idno type="halauthorid">604717</idno> <affiliation ref="#struct-132603"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Guido</forename> <surname>Alves</surname> </persName> <idno type="halauthorid">604718</idno> <affiliation ref="#struct-154503"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Henrik</forename> <surname>Zetterberg</surname> </persName> <idno type="halauthorid">517696</idno> <affiliation ref="#struct-154504"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Kaj</forename> <surname>Blennow</surname> </persName> <idno type="halauthorid">517702</idno> <affiliation ref="#struct-154504"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Ragnhild</forename> <surname>Skogseth</surname> </persName> <idno type="halauthorid">604719</idno> <affiliation ref="#struct-50793"></affiliation> </author> <author role="aut"> <persName> <forename type="first">Lennart</forename> <surname>Minthon</surname> </persName> <idno type="halauthorid">604720</idno> <affiliation ref="#struct-154501"></affiliation> </author> <author role="crp"> <persName> <forename type="first">Dag</forename> <surname>Aarsland</surname> </persName> <email type="md5">95349a6f8c012fa9f41d8aa7417ff0a8</email> <email type="domain">gmail.com</email> <idno type="halauthorid">564338</idno> <affiliation ref="#struct-154505"></affiliation> </author> </analytic> <monogr> <idno type="halJournalId" status="VALID">15872</idno> <idno type="issn">0022-3050</idno> <idno type="eissn">1468-330X</idno> <title level="j">Journal of Neurology, Neurosurgery and Psychiatry</title> <imprint> <publisher>BMJ Publishing Group</publisher> <biblScope unit="volume">82</biblScope> <biblScope unit="issue">2</biblScope> <biblScope unit="pp">160</biblScope> <date type="datePub">2010-11-03</date> </imprint> </monogr> <idno type="doi">10.1136/jnnp.2009.199398</idno> </biblStruct> </sourceDesc> <profileDesc> <langUsage> <language ident="en">English</language> </langUsage> <textClass> <keywords scheme="author"> <term xml:lang="en">ALZHEIMER'S DISEASE</term> <term xml:lang="en">DEMENTIA</term> <term xml:lang="en">LEWY BODY</term> <term xml:lang="en">PARKINSON'S DISEASE</term> </keywords> <classCode scheme="halTypology" n="ART">Journal articles</classCode> </textClass> <abstract xml:lang="en">Background The clinical distinction between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is sometimes difficult, particularly in mild cases. Although cerebrospinal fluid (CSF) markers such as Aβ42 and P-tau can distinguish between AD and normal controls, their ability to distinguish between AD and DLB is not adequate. Objective This study aims at investigating whether CSF markers, in particular the level of Aβ38, can differentiate between mild AD and DLB. Methods In total 85 individuals were included after standardized diagnostic procedures: 30 diagnosed as probable AD, 23 probable DLB, 20 with probable Parkinson's disease dementia (PDD), and 12 non-demented controls subjects. CSF levels of Aβ38, Aβ40 and Aβ42 were determined using commercially available Ultra-Sensitive multi-array kit assay (MSD) for human Aβ peptides. Total-tau (T-tau) and Phosphorylated tau (P-Tau) were analysed using ELISA (Innotest). In addition, combinations (Aβ42/Aβ38, Aβ42/Aβ40, Aβ42/P-tau, and Aβ42/Aβ38/P-tau) were assessed. Results Significant between-group differences were found for all CSF measures, and all except Aβ40, Aβ42, and Aβ42/P-tau differed between AD and DLB. Aβ42/Aβ38 ratio was the measure that best discriminated between AD and DLB (AUC 0.781; p<0.005), with sensitivity 74% and specificity 77%. Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy. Studies with independent and larger samples and a priori cut-offs are needed to test this hypothesis.</abstract> </profileDesc> </hal></record>Pour manipuler ce document sous Unix (Dilib)
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