Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers
Identifieur interne : 001589 ( Main/Corpus ); précédent : 001588; suivant : 001590Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers
Auteurs : Kathrin Brockmann ; Adriane Gröger ; Adriana Di Santo ; Inga Liepelt ; Claudia Schulte ; Uwe Klose ; Walter Maetzler ; Ann-Kathrin Hauser ; Ruediger Hilker ; Baltazar Gomez-Mancilla ; Daniela Berg ; Thomas GasserSource :
- Movement Disorders [ 0885-3185 ] ; 2011-11.
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Abstract
The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic LRRK2 patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic LRRK2 mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. LRRK2 patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in LRRK2 patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic LRRK2 mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic LRRK2 mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in LRRK2 patients and of the cuneus in asymptomatic LRRK2 mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in LRRK2 patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in LRRK2 patients and asymptomatic LRRK2 mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in LRRK2 mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected LRRK2 mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23991
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers</title><author><name sortKey="Brockmann, Kathrin" sort="Brockmann, Kathrin" uniqKey="Brockmann K" first="Kathrin" last="Brockmann">Kathrin Brockmann</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Groger, Adriane" sort="Groger, Adriane" uniqKey="Groger A" first="Adriane" last="Gröger">Adriane Gröger</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Di Santo, Adriana" sort="Di Santo, Adriana" uniqKey="Di Santo A" first="Adriana" last="Di Santo">Adriana Di Santo</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Liepelt, Inga" sort="Liepelt, Inga" uniqKey="Liepelt I" first="Inga" last="Liepelt">Inga Liepelt</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schulte, Claudia" sort="Schulte, Claudia" uniqKey="Schulte C" first="Claudia" last="Schulte">Claudia 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Germany</mods:affiliation></affiliation></author><author><name sortKey="Hauser, Ann Athrin" sort="Hauser, Ann Athrin" uniqKey="Hauser A" first="Ann-Kathrin" last="Hauser">Ann-Kathrin Hauser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hilker, Ruediger" sort="Hilker, Ruediger" uniqKey="Hilker R" first="Ruediger" last="Hilker">Ruediger Hilker</name><affiliation><mods:affiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gomez Ancilla, Baltazar" sort="Gomez Ancilla, Baltazar" uniqKey="Gomez Ancilla B" first="Baltazar" last="Gomez-Mancilla">Baltazar Gomez-Mancilla</name><affiliation><mods:affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:5A76C63496F4331945E9911BA71520E3F70B4438</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23991</idno><idno type="url">https://api.istex.fr/document/5A76C63496F4331945E9911BA71520E3F70B4438/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001589</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers</title><author><name sortKey="Brockmann, Kathrin" sort="Brockmann, Kathrin" uniqKey="Brockmann K" first="Kathrin" last="Brockmann">Kathrin Brockmann</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Groger, Adriane" sort="Groger, Adriane" uniqKey="Groger A" first="Adriane" last="Gröger">Adriane Gröger</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Di Santo, Adriana" sort="Di Santo, Adriana" uniqKey="Di Santo A" first="Adriana" last="Di Santo">Adriana Di Santo</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Liepelt, Inga" sort="Liepelt, Inga" uniqKey="Liepelt I" first="Inga" last="Liepelt">Inga Liepelt</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Schulte, Claudia" sort="Schulte, Claudia" uniqKey="Schulte C" first="Claudia" last="Schulte">Claudia Schulte</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klose, Uwe" sort="Klose, Uwe" uniqKey="Klose U" first="Uwe" last="Klose">Uwe Klose</name><affiliation><mods:affiliation>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Maetzler, Walter" sort="Maetzler, Walter" uniqKey="Maetzler W" first="Walter" last="Maetzler">Walter Maetzler</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hauser, Ann Athrin" sort="Hauser, Ann Athrin" uniqKey="Hauser A" first="Ann-Kathrin" last="Hauser">Ann-Kathrin Hauser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hilker, Ruediger" sort="Hilker, Ruediger" uniqKey="Hilker R" first="Ruediger" last="Hilker">Ruediger Hilker</name><affiliation><mods:affiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gomez Ancilla, Baltazar" sort="Gomez Ancilla, Baltazar" uniqKey="Gomez Ancilla B" first="Baltazar" last="Gomez-Mancilla">Baltazar Gomez-Mancilla</name><affiliation><mods:affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-11">2011-11</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="2335">2335</biblScope><biblScope unit="page" to="2342">2342</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">5A76C63496F4331945E9911BA71520E3F70B4438</idno><idno type="DOI">10.1002/mds.23991</idno><idno type="ArticleID">MDS23991</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>LRRK2</term><term>MRI</term><term>TCS</term><term>monogenic Parkinson</term><term>motor network</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic LRRK2 patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic LRRK2 mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. LRRK2 patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in LRRK2 patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic LRRK2 mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic LRRK2 mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in LRRK2 patients and of the cuneus in asymptomatic LRRK2 mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in LRRK2 patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in LRRK2 patients and asymptomatic LRRK2 mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in LRRK2 mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected LRRK2 mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Kathrin Brockmann MD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string><json:string>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</json:string></affiliations></json:item><json:item><name>Adriane Gröger PhD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Adriana Di Santo MD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Inga Liepelt PhD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string><json:string>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</json:string></affiliations></json:item><json:item><name>Claudia Schulte PhD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Uwe Klose PhD</name><affiliations><json:string>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Walter Maetzler MD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string><json:string>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</json:string></affiliations></json:item><json:item><name>Ann‐Kathrin Hauser</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string></affiliations></json:item><json:item><name>Ruediger Hilker MD</name><affiliations><json:string>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Baltazar Gomez‐Mancilla PhD</name><affiliations><json:string>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</json:string></affiliations></json:item><json:item><name>Daniela Berg MD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string><json:string>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</json:string></affiliations></json:item><json:item><name>Thomas Gasser MD</name><affiliations><json:string>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</json:string><json:string>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>monogenic Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LRRK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor network</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MRI</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TCS</value></json:item></subject><articleId><json:string>MDS23991</json:string></articleId><language><json:string>eng</json:string></language><abstract>The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic LRRK2 patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic LRRK2 mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. LRRK2 patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in LRRK2 patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic LRRK2 mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic LRRK2 mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in LRRK2 patients and of the cuneus in asymptomatic LRRK2 mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in LRRK2 patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in LRRK2 patients and asymptomatic LRRK2 mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in LRRK2 mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected LRRK2 mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.539</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1937</abstractCharCount><pdfWordCount>4539</pdfWordCount><pdfCharCount>30391</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>262</abstractWordCount></qualityIndicators><title>Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation 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carriers</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: This study was supported by Novartis Pharma AG.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers</title><author><persName><forename type="first">Kathrin</forename><surname>Brockmann</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurodegeneration, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Str. 3, D ‐ 72076 Tübingen, Germany</p></note><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation></author><author><persName><forename type="first">Adriane</forename><surname>Gröger</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Adriana</forename><surname>Di Santo</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Inga</forename><surname>Liepelt</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation></author><author><persName><forename type="first">Claudia</forename><surname>Schulte</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Uwe</forename><surname>Klose</surname></persName><roleName type="degree">PhD</roleName><affiliation>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Walter</forename><surname>Maetzler</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation></author><author><persName><forename type="first">Ann‐Kathrin</forename><surname>Hauser</surname></persName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation></author><author><persName><forename type="first">Ruediger</forename><surname>Hilker</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Baltazar</forename><surname>Gomez‐Mancilla</surname></persName><roleName type="degree">PhD</roleName><affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</affiliation></author><author><persName><forename type="first">Daniela</forename><surname>Berg</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Gasser</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-11"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="2335">2335</biblScope><biblScope unit="page" to="2342">2342</biblScope></imprint></monogr><idno type="istex">5A76C63496F4331945E9911BA71520E3F70B4438</idno><idno type="DOI">10.1002/mds.23991</idno><idno type="ArticleID">MDS23991</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic LRRK2 patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic LRRK2 mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. LRRK2 patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in LRRK2 patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic LRRK2 mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic LRRK2 mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in LRRK2 patients and of the cuneus in asymptomatic LRRK2 mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in LRRK2 patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in LRRK2 patients and asymptomatic LRRK2 mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in LRRK2 mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected LRRK2 mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>monogenic Parkinson</term></item><item><term>LRRK2</term></item><item><term>motor network</term></item><item><term>MRI</term></item><item><term>TCS</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="2010-12-30">Received</change><change when="2011-08-29">Registration</change><change when="2011-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5A76C63496F4331945E9911BA71520E3F70B4438/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="130"><doi origin="wiley" registered="yes">10.1002/mds.v26.13</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">13</numbering></numberingGroup><coverDate startDate="2011-11">November 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="70" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23991</doi><idGroup><id type="unit" value="MDS23991"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-12-30"></event><event type="manuscriptRevised" date="2011-08-13"></event><event 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href="file:MDS.MDS23991.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="46"></count><count type="wordTotal" number="6696"></count></countGroup><titleGroup><title type="main" xml:lang="en">Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers<link href="#fn1"></link><link href="#fn2"></link><link href="#fn3"></link></title><title type="short" xml:lang="en">Motor Network Reorganization in LRRK2</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Kathrin</givenNames><familyName>Brockmann</familyName><degrees>MD</degrees></personName><contactDetails><email normalForm="Kathrin.Brockmann@uni-tuebingen.de">Kathrin.Brockmann@uni‐tuebingen.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Adriane</givenNames><familyName>Gröger</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Adriana</givenNames><familyName>Di Santo</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Inga</givenNames><familyName>Liepelt</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Claudia</givenNames><familyName>Schulte</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Uwe</givenNames><familyName>Klose</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Walter</givenNames><familyName>Maetzler</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ann‐Kathrin</givenNames><familyName>Hauser</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Ruediger</givenNames><familyName>Hilker</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Baltazar</givenNames><familyName>Gomez‐Mancilla</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Daniela</givenNames><familyName>Berg</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Thomas</givenNames><familyName>Gasser</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="CH" type="organization"><unparsedAffiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">monogenic Parkinson</keyword><keyword xml:id="kwd2">LRRK2</keyword><keyword xml:id="kwd3">motor network</keyword><keyword xml:id="kwd4">MRI</keyword><keyword xml:id="kwd5">TCS</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23991:MDS_23991_sm_SuppInfo"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic <i>LRRK2</i> patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic <i>LRRK2</i> mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. <i>LRRK2</i> patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in <i>LRRK2</i> patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic <i>LRRK2</i> mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic <i>LRRK2</i> mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in <i>LRRK2</i> patients and of the cuneus in asymptomatic <i>LRRK2</i> mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in <i>LRRK2</i> patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in <i>LRRK2</i> patients and asymptomatic <i>LRRK2</i> mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in <i>LRRK2</i> mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected <i>LRRK2</i> mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Funding agencies</b>: This study was supported by Novartis Pharma AG.</p></note><note xml:id="fn2"><p><b>Relevant conflicts of interest/financial disclosures</b>: Nothing to report.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Motor Network Reorganization in LRRK2</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers</title></titleInfo><name type="personal"><namePart type="given">Kathrin</namePart><namePart type="family">Brockmann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation><description>Correspondence: Department of Neurodegeneration, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Str. 3, D ‐ 72076 Tübingen, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adriane</namePart><namePart type="family">Gröger</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Adriana</namePart><namePart type="family">Di Santo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Inga</namePart><namePart type="family">Liepelt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Schulte</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Uwe</namePart><namePart type="family">Klose</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter</namePart><namePart type="family">Maetzler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ann‐Kathrin</namePart><namePart type="family">Hauser</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ruediger</namePart><namePart type="family">Hilker</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Baltazar</namePart><namePart type="family">Gomez‐Mancilla</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniela</namePart><namePart type="family">Berg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Gasser</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-11</dateIssued><dateCaptured encoding="w3cdtf">2010-12-30</dateCaptured><dateValid encoding="w3cdtf">2011-08-29</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">2</extent><extent unit="references">46</extent><extent unit="words">6696</extent></physicalDescription><abstract lang="en">The objective of this research was to evaluate a possible endophenotype in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). Ten symptomatic LRRK2 patients, 24 sporadic Parkinson's disease patients as well as 10 asymptomatic LRRK2 mutation carriers and 29 matched healthy controls underwent comprehensive clinical assessments with respect to motor and non‐motor symptoms. Transcranial sonography and magnetic resonance imaging (voxel‐based morphometry [VBM]) were assessed to evaluate morphological imaging characteristics. LRRK2 patients had an earlier onset of motor symptoms and a more benign phenotype of motor and non‐motor characteristics compared to sporadic Parkinson's disease patients. However, depression scores were higher in LRRK2 patients. No clinical differences were found regarding motor and non‐motor symptoms in asymptomatic LRRK2 mutation carriers in comparison to controls. Transcranial sonography showed hyperechogenicity of the substantia nigra in both patients' cohorts as well as in asymptomatic LRRK2 mutation carriers. Voxel‐based morphometry revealed increased gray matter volume of the cerebellum and precentral gyrus in LRRK2 patients and of the cuneus in asymptomatic LRRK2 mutation carriers. In contrast, we found decreased basal ganglia gray matter volume in LRRK2 patients compared to controls. Increased gray matter volume of different anatomical structures associated with motor loops in LRRK2 patients and asymptomatic LRRK2 mutation carriers compared to age‐matched sporadic Parkinson's disease patients and controls might indicate compensatory mechanism in LRRK2 mutation carriers due to motor network plasticity not only in the symptomatic stage of the disease but even in the premotor phase. Substantia nigra hyperechogenicity in yet unaffected LRRK2 mutation carriers indicates morphologic alterations in an asymptomatic stage of disease. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: This study was supported by Novartis Pharma AG.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>monogenic Parkinson</topic><topic>LRRK2</topic><topic>motor network</topic><topic>MRI</topic><topic>TCS</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - </note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>13</number></detail><extent unit="pages"><start>2335</start><end>2342</end><total>8</total></extent></part></relatedItem><identifier type="istex">5A76C63496F4331945E9911BA71520E3F70B4438</identifier><identifier type="DOI">10.1002/mds.23991</identifier><identifier type="ArticleID">MDS23991</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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