Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers
Identifieur interne : 001356 ( Main/Curation ); précédent : 001355; suivant : 001357Clinical and brain imaging characteristics in leucine‐rich repeat kinase 2–associated PD and asymptomatic mutation carriers
Auteurs : Kathrin Brockmann [Allemagne] ; Adriane Gröger [Allemagne] ; Adriana Di Santo [Allemagne] ; Inga Liepelt [Allemagne] ; Claudia Schulte [Allemagne] ; Uwe Klose [Allemagne] ; Walter Maetzler [Allemagne] ; Ann-Kathrin Hauser [Allemagne] ; Ruediger Hilker [Allemagne] ; Baltazar Gomez-Mancilla [Suisse] ; Daniela Berg [Allemagne] ; Thomas Gasser [Allemagne]Source :
- 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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Frankfurt</wicri:regionArea></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 wicri:level="1"><mods:affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</mods:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Novartis Institute of Biomedical Research at Novartis, Basel</wicri:regionArea></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, 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Brockmann</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Neurodegenerative Diseases (DZNE), Bonn</wicri:regionArea></affiliation></author><author><name sortKey="Groger, Adriane" sort="Groger, Adriane" uniqKey="Groger A" first="Adriane" last="Gröger">Adriane Gröger</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></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 wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation></author><author><name sortKey="Liepelt, Inga" sort="Liepelt, Inga" uniqKey="Liepelt I" first="Inga" last="Liepelt">Inga Liepelt</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Neurodegenerative Diseases (DZNE), Bonn</wicri:regionArea></affiliation></author><author><name sortKey="Schulte, Claudia" sort="Schulte, Claudia" uniqKey="Schulte C" first="Claudia" last="Schulte">Claudia Schulte</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation></author><author><name sortKey="Klose, Uwe" sort="Klose, Uwe" uniqKey="Klose U" first="Uwe" last="Klose">Uwe Klose</name><affiliation wicri:level="1"><mods:affiliation>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>MR‐Research Group, Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen</wicri:regionArea></affiliation></author><author><name sortKey="Maetzler, Walter" sort="Maetzler, Walter" uniqKey="Maetzler W" first="Walter" last="Maetzler">Walter Maetzler</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Neurodegenerative Diseases (DZNE), Bonn</wicri:regionArea></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 wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation></author><author><name sortKey="Hilker, Ruediger" sort="Hilker, Ruediger" uniqKey="Hilker R" first="Ruediger" last="Hilker">Ruediger Hilker</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology and Brain Imaging Center, University of Frankfurt, Frankfurt</wicri:regionArea></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 wicri:level="1"><mods:affiliation>Novartis Institute of Biomedical Research at Novartis, Basel, Switzerland</mods:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Novartis Institute of Biomedical Research at Novartis, Basel</wicri:regionArea></affiliation></author><author><name sortKey="Berg, Daniela" sort="Berg, Daniela" uniqKey="Berg D" first="Daniela" last="Berg">Daniela Berg</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Neurodegenerative Diseases (DZNE), Bonn</wicri:regionArea></affiliation></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Neurodegenerative Diseases (DZNE), Bonn</wicri:regionArea></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></record>Pour manipuler ce document sous Unix (Dilib)
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