The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia
Identifieur interne : 003169 ( Main/Corpus ); précédent : 003168; suivant : 003170The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia
Auteurs : M. Andersson ; H. Zetterberg ; L. Minthon ; K. Blennow ; E. LondosSource :
- International Journal of Geriatric Psychiatry [ 0885-6230 ] ; 2011-01.
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- KwdEn :
Abstract
Objective: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD. Methods: Clinically diagnosed DLB (n = 47) and PDD (n = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ181) and the 42 amino acid isoform of amyloid β, Aβ42 were determined. Results: We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE. Conclusion: The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. Copyright © 2010 John Wiley & Sons, Ltd.
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DOI: 10.1002/gps.2496
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Zetterberg</name><affiliation><mods:affiliation>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Minthon, L" sort="Minthon, L" uniqKey="Minthon L" first="L." last="Minthon">L. Minthon</name><affiliation><mods:affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</mods:affiliation></affiliation><affiliation><mods:affiliation>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Blennow, K" sort="Blennow, K" uniqKey="Blennow K" first="K." last="Blennow">K. 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Londos</name><affiliation><mods:affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A2786702C1D18202BB547706F04EA5C85085ABEC</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/gps.2496</idno><idno type="url">https://api.istex.fr/document/A2786702C1D18202BB547706F04EA5C85085ABEC/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">003169</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia</title><author><name sortKey="Andersson, M" sort="Andersson, M" uniqKey="Andersson M" first="M." last="Andersson">M. Andersson</name><affiliation><mods:affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</mods:affiliation></affiliation><affiliation><mods:affiliation>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Zetterberg, H" sort="Zetterberg, H" uniqKey="Zetterberg H" first="H." last="Zetterberg">H. Zetterberg</name><affiliation><mods:affiliation>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Minthon, L" sort="Minthon, L" uniqKey="Minthon L" first="L." last="Minthon">L. Minthon</name><affiliation><mods:affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</mods:affiliation></affiliation><affiliation><mods:affiliation>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Blennow, K" sort="Blennow, K" uniqKey="Blennow K" first="K." last="Blennow">K. Blennow</name><affiliation><mods:affiliation>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Londos, E" sort="Londos, E" uniqKey="Londos E" first="E." last="Londos">E. Londos</name><affiliation><mods:affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">International Journal of Geriatric Psychiatry</title><title level="j" type="abbrev">Int. J. Geriat. Psychiatry</title><idno type="ISSN">0885-6230</idno><idno type="eISSN">1099-1166</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2011-01">2011-01</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="100">100</biblScope><biblScope unit="page" to="105">105</biblScope></imprint><idno type="ISSN">0885-6230</idno></series><idno type="istex">A2786702C1D18202BB547706F04EA5C85085ABEC</idno><idno type="DOI">10.1002/gps.2496</idno><idno type="ArticleID">GPS2496</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-6230</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer's disease</term><term>CSF biomarkers</term><term>Lewy body disease</term><term>MMSE</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD. Methods: Clinically diagnosed DLB (n = 47) and PDD (n = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ181) and the 42 amino acid isoform of amyloid β, Aβ42 were determined. Results: We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE. Conclusion: The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. Copyright © 2010 John Wiley & Sons, Ltd.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. Andersson</name><affiliations><json:string>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</json:string><json:string>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</json:string></affiliations></json:item><json:item><name>H. Zetterberg</name><affiliations><json:string>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</json:string></affiliations></json:item><json:item><name>L. Minthon</name><affiliations><json:string>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</json:string><json:string>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</json:string></affiliations></json:item><json:item><name>K. Blennow</name><affiliations><json:string>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</json:string></affiliations></json:item><json:item><name>E. Londos</name><affiliations><json:string>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Lewy body disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CSF biomarkers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MMSE</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item></subject><articleId><json:string>GPS2496</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD. Methods: Clinically diagnosed DLB (n = 47) and PDD (n = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ181) and the 42 amino acid isoform of amyloid β, Aβ42 were determined. Results: We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE. Conclusion: The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. 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J. Geriat. Psychiatry</title><idno type="pISSN">0885-6230</idno><idno type="eISSN">1099-1166</idno><idno type="DOI">10.1002/(ISSN)1099-1166</idno><imprint><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2011-01"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="100">100</biblScope><biblScope unit="page" to="105">105</biblScope></imprint></monogr><idno type="istex">A2786702C1D18202BB547706F04EA5C85085ABEC</idno><idno type="DOI">10.1002/gps.2496</idno><idno type="ArticleID">GPS2496</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD. Methods: Clinically diagnosed DLB (n = 47) and PDD (n = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ181) and the 42 amino acid isoform of amyloid β, Aβ42 were determined. Results: We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE. Conclusion: The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. Copyright © 2010 John Wiley & Sons, Ltd.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Lewy body disease</term></item><item><term>CSF biomarkers</term></item><item><term>MMSE</term></item><item><term>Alzheimer's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-11-18">Received</change><change when="2010-01-14">Registration</change><change when="2011-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A2786702C1D18202BB547706F04EA5C85085ABEC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd.</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1099-1166</doi><issn type="print">0885-6230</issn><issn type="electronic">1099-1166</issn><idGroup><id type="product" value="GPS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY">International Journal of Geriatric Psychiatry</title><title type="short">Int. 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An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>Clinically diagnosed DLB (<i>n</i> = 47) and PDD (<i>n</i> = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ<sub>181</sub>) and the 42 amino acid isoform of amyloid β, Aβ42 were determined.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE.</p></section><section xml:id="abs1-4"><title type="main">Conclusion</title><p>The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. Copyright © 2010 John Wiley & Sons, Ltd.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MMSE profile and CSF biomarkers</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Andersson</namePart><affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</affiliation><affiliation>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Zetterberg</namePart><affiliation>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Minthon</namePart><affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</affiliation><affiliation>Clinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Blennow</namePart><affiliation>Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Londos</namePart><affiliation>Neuropsychiatric clinic, Malmö University Hospital, Malmö, Sweden</affiliation><description>Correspondence: Neuropsychiatric clinic, Malmö University Hospital, Malmö Sweden.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Ltd.</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-01</dateIssued><dateCaptured encoding="w3cdtf">2009-11-18</dateCaptured><dateValid encoding="w3cdtf">2010-01-14</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">3</extent><extent unit="references">29</extent></physicalDescription><abstract lang="en">Objective: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer's disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD. Methods: Clinically diagnosed DLB (n = 47) and PDD (n = 17) patients from a clinical follow‐up programme were investigated. All performed mini mental state examination (MMSE) and went through lumbar puncture at baseline. CSF concentrations of total τ (T‐τ), τ phosphorylated at threonine 181 (P‐τ181) and the 42 amino acid isoform of amyloid β, Aβ42 were determined. Results: We found significant differences in T‐τ and Aβ42, with a higher level of T‐τ and a lower level of Aβ42 in DLB compared to PDD. The combination of T‐τ with Aβ42 showed better discrimination between DLB and PDD than either of the measures alone. In DLB, a CSF profile more like the one seen in AD was significantly correlated with worse performance on the orientation and memory of the MMSE. Conclusion: The correlation suggests a possible link between a higher degree of AD pathology and a profile of more temporal disabilities on cognitive tests in DLB. This might aid in identifying a subgroup of patients with a greater burden of AD pathology in a clinical setting and could have important implications for prognosis. Copyright © 2010 John Wiley & Sons, Ltd.</abstract><subject lang="en"><genre>Keywords</genre><topic>Lewy body disease</topic><topic>CSF biomarkers</topic><topic>MMSE</topic><topic>Alzheimer's disease</topic></subject><relatedItem type="host"><titleInfo><title>International Journal of Geriatric Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>Int. J. Geriat. Psychiatry</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-6230</identifier><identifier type="eISSN">1099-1166</identifier><identifier type="DOI">10.1002/(ISSN)1099-1166</identifier><identifier type="PublisherID">GPS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>100</start><end>105</end><total>6</total></extent></part></relatedItem><identifier type="istex">A2786702C1D18202BB547706F04EA5C85085ABEC</identifier><identifier type="DOI">10.1002/gps.2496</identifier><identifier type="ArticleID">GPS2496</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 John Wiley & Sons, Ltd.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Ltd.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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