La maladie de Parkinson au Canada (serveur d'exploration)

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Behavioral deficits and striatal DA signaling in LRRK2 p.G2019S transgenic rats: a multimodal investigation including PET neuroimaging.

Identifieur interne : 000B35 ( Main/Exploration ); précédent : 000B34; suivant : 000B36

Behavioral deficits and striatal DA signaling in LRRK2 p.G2019S transgenic rats: a multimodal investigation including PET neuroimaging.

Auteurs : Matthew D. Walker [Canada] ; Mattia Volta [Canada] ; Stefano Cataldi [Canada] ; Katherine Dinelle [Canada] ; Dayne Beccano-Kelly [Canada] ; Lise Munsie [Canada] ; Rick Kornelsen [Canada] ; Chenoa Mah [Canada] ; Patrick Chou [Canada] ; Kimberley Co [Canada] ; Jaskaran Khinda [Canada] ; Marta Mroczek [Canada] ; Sabrina Bergeron [Canada] ; Katrina Yu [Canada] ; Li Ping Cao [Canada] ; Natalja Funk [Allemagne] ; Thomas Ott [Allemagne] ; Dagmar Galter [Suède] ; Olaf Riess [Allemagne] ; Saskia Biskup [Allemagne] ; Austen J. Milnerwood [Canada] ; A Jon Stoessl [Canada] ; Matthew J. Farrer [Canada] ; Vesna Sossi [Canada]

Source :

RBID : pubmed:25000966

English descriptors

Abstract

A major risk-factor for developing Parkinson's disease (PD) is genetic variability in leucine-rich repeat kinase 2 (LRRK2), most notably the p.G2019S mutation. Examination of the effects of this mutation is necessary to determine the etiology of PD and to guide therapeutic development.

DOI: 10.3233/JPD-140344
PubMed: 25000966


Affiliations:


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Le document en format XML

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<wicri:regionArea>Department of Neurodegeneration, Hertie Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases DZNE, Tübingen</wicri:regionArea>
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<wicri:regionArea>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, BC</wicri:regionArea>
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<name sortKey="Farrer, Matthew J" sort="Farrer, Matthew J" uniqKey="Farrer M" first="Matthew J" last="Farrer">Matthew J. Farrer</name>
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<title level="j">Journal of Parkinson's disease</title>
<idno type="eISSN">1877-718X</idno>
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<date when="2014" type="published">2014</date>
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<term>Animals</term>
<term>Brain (diagnostic imaging)</term>
<term>Brain (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Dopamine (metabolism)</term>
<term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term>
<term>Dopamine and cAMP-Regulated Phosphoprotein 32 (metabolism)</term>
<term>Humans</term>
<term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term>
<term>Male</term>
<term>Motor Activity (genetics)</term>
<term>Neostriatum (diagnostic imaging)</term>
<term>Neostriatum (metabolism)</term>
<term>Parkinson Disease (genetics)</term>
<term>Phosphorylation</term>
<term>Positron-Emission Tomography</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Rats, Transgenic</term>
<term>Receptors, Dopamine D2 (metabolism)</term>
<term>Rotarod Performance Test</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>Vesicular Monoamine Transport Proteins (metabolism)</term>
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<term>Protein-Serine-Threonine Kinases</term>
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<term>Dopamine Plasma Membrane Transport Proteins</term>
<term>Dopamine and cAMP-Regulated Phosphoprotein 32</term>
<term>Receptors, Dopamine D2</term>
<term>Tyrosine 3-Monooxygenase</term>
<term>Vesicular Monoamine Transport Proteins</term>
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<term>Brain</term>
<term>Neostriatum</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Motor Activity</term>
<term>Parkinson Disease</term>
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<term>Brain</term>
<term>Neostriatum</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Disease Models, Animal</term>
<term>Humans</term>
<term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term>
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<front>
<div type="abstract" xml:lang="en">A major risk-factor for developing Parkinson's disease (PD) is genetic variability in leucine-rich repeat kinase 2 (LRRK2), most notably the p.G2019S mutation. Examination of the effects of this mutation is necessary to determine the etiology of PD and to guide therapeutic development.</div>
</front>
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<name sortKey="Kornelsen, Rick" sort="Kornelsen, Rick" uniqKey="Kornelsen R" first="Rick" last="Kornelsen">Rick Kornelsen</name>
<name sortKey="Mah, Chenoa" sort="Mah, Chenoa" uniqKey="Mah C" first="Chenoa" last="Mah">Chenoa Mah</name>
<name sortKey="Milnerwood, Austen J" sort="Milnerwood, Austen J" uniqKey="Milnerwood A" first="Austen J" last="Milnerwood">Austen J. Milnerwood</name>
<name sortKey="Mroczek, Marta" sort="Mroczek, Marta" uniqKey="Mroczek M" first="Marta" last="Mroczek">Marta Mroczek</name>
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<name sortKey="Yu, Katrina" sort="Yu, Katrina" uniqKey="Yu K" first="Katrina" last="Yu">Katrina Yu</name>
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<name sortKey="Ott, Thomas" sort="Ott, Thomas" uniqKey="Ott T" first="Thomas" last="Ott">Thomas Ott</name>
<name sortKey="Riess, Olaf" sort="Riess, Olaf" uniqKey="Riess O" first="Olaf" last="Riess">Olaf Riess</name>
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<name sortKey="Galter, Dagmar" sort="Galter, Dagmar" uniqKey="Galter D" first="Dagmar" last="Galter">Dagmar Galter</name>
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