PET in LRRK2 mutations: comparison to sporadic Parkinson's disease and evidence for presymptomatic compensation
Identifieur interne : 002A37 ( Main/Exploration ); précédent : 002A36; suivant : 002A38PET in LRRK2 mutations: comparison to sporadic Parkinson's disease and evidence for presymptomatic compensation
Auteurs : John R. Adams ; Hinke Van Netten ; Michael Schulzer ; Edwin Mak ; Jessamyn Mckenzie ; Audrey Strongosky [États-Unis] ; Vesna Sossi ; Thomas J. Ruth ; Chong S. Lee ; Matthew Farrer [États-Unis] ; Thomas Gasser [Allemagne] ; Ryan J. Uitti [États-Unis] ; Donald B. Calne ; Zbigniew K. Wszolek [États-Unis] ; A. Jon StoesslSource :
- Brain [ 0006-8950 ] ; 2005-12.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- 11C-DTBZ = 11C-(±)α-dihydrotetrabenazine, 11C-MP = 11C-d-threo-methylphenidate, 11C-RAC = 11C-raclopride, 18F-dopa = 18F-6-fluoro-l-dopa, Adult, Age Factors, Aged, BP = binding potential, Brain (diagnostic imaging), Brain (metabolism), Carbon Radioisotopes, Carboxy-Lyases (metabolism), Case-Control Studies, Comparative study, Compensation, DAT = dopamine transporter, Dopamine Plasma Membrane Transport Proteins (metabolism), Emission tomography, Fluorine Radioisotopes, Humans, Image Processing, Computer-Assisted, LRRK2 = leucine-rich repeat kinase 2, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Levodopa (metabolism), Methylphenidate, Middle Aged, Mutation, Nervous system diseases, PET = positron emission tomography, Parkinson Disease (diagnostic imaging), Parkinson Disease (genetics), Parkinson disease, Parkinson's disease, Pathophysiology, Phenotype, Positron, Positron emission tomography, Positron-Emission Tomography, Protein-Serine-Threonine Kinases (genetics), Radiopharmaceuticals, Receptors, Dopamine D2 (metabolism), Regression Analysis, Sporadic, Tetrabenazine (analogs & derivatives), Tetrabenazine (metabolism), UPDRS = Unified Parkinson's Disease Rating Scale, VMAT2 = vesicular monoamine transporter, genetics, pathophysiology, positron emission tomography, sPD = sporadic Parkinson's disease.
- MESH :
- chemical , analogs & derivatives : Tetrabenazine.
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Carboxy-Lyases, Dopamine Plasma Membrane Transport Proteins, Levodopa, Receptors, Dopamine D2, Tetrabenazine.
- chemical : Carbon Radioisotopes, Fluorine Radioisotopes, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Methylphenidate, Radiopharmaceuticals.
- diagnostic imaging : Brain, Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Brain.
- Adult, Age Factors, Aged, Case-Control Studies, Humans, Image Processing, Computer-Assisted, Middle Aged, Mutation, Phenotype, Positron-Emission Tomography, Regression Analysis.
Abstract
Parkinson's disease may arise from multiple aetiologies, including genetic mutations that are for the most part uncommon. We describe here the positron emission tomography (PET) findings in clinically affected and asymptomatic, high-risk members of two autosomal dominantly inherited Parkinson's disease kindreds with recently described mutations at the PARK8 locus, in a novel gene encoding a leucine-rich repeat kinase (LRRK2). Affected family members have l-dopa-responsive parkinsonism with loss of dopaminergic nigral neurons and pleomorphic subcellular pathology. Fifteen family members underwent PET using: 18F-6-fluoro-l-dopa (18F-dopa) to assess dopamine (DA) synthesis and storage, 11C-(±)α-dihydrotetrabenazine (11C-DTBZ) for the vesicular monoamine transporter, and 11C-d-threo-methylphenidate (11C-MP) for the membrane dopamine transporter (DAT). Measurements were compared with normal (n = 33) and sporadic Parkinson's disease (sPD) (n = 67) control groups. Four clinically affected members had findings similar to sPD, with impaired presynaptic DA function affecting the putamen more than the caudate. In two affected members, D2 dopamine receptor binding was intact. Two asymptomatic mutation carriers had abnormal DAT binding with another two developing such abnormalities over 4 years of follow-up. In these individuals, 18F-dopa uptake remained normal, although two of them also displayed abnormal 11C-DTBZ binding. Our study demonstrates that the in vivo neurochemical phenotype of LRRK2 mutations is indistinguishable from that of sPD, despite the pathological heterogeneity of the condition. Furthermore, we suggest that compensatory changes including downregulation of the DAT and upregulation of decarboxylase activity may delay the onset of parkinsonian symptoms.
Url:
DOI: 10.1093/brain/awh607
Affiliations:
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Adams</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Van Netten, Hinke" sort="Van Netten, Hinke" uniqKey="Van Netten H" first="Hinke" last="Van Netten">Hinke Van Netten</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Mak, Edwin" sort="Mak, Edwin" uniqKey="Mak E" first="Edwin" last="Mak">Edwin Mak</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Mckenzie, Jessamyn" sort="Mckenzie, Jessamyn" uniqKey="Mckenzie J" first="Jessamyn" last="Mckenzie">Jessamyn Mckenzie</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Strongosky, Audrey" sort="Strongosky, Audrey" uniqKey="Strongosky A" first="Audrey" last="Strongosky">Audrey Strongosky</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Mayo Clinic, Jacksonville, FL</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J." last="Ruth">Thomas J. Ruth</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S." last="Lee">Chong S. Lee</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Mayo Clinic, Jacksonville, FL</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurodegenerative disorders, Hertie Institute for Clinical Brain Research, Center of Neurology, University of Tubingen, Tubingen</wicri:regionArea><wicri:noRegion>Tubingen</wicri:noRegion><wicri:noRegion>Tubingen</wicri:noRegion></affiliation><affiliation></affiliation></author><author><name sortKey="Uitti, Ryan J" sort="Uitti, Ryan J" uniqKey="Uitti R" first="Ryan J." last="Uitti">Ryan J. Uitti</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Mayo Clinic, Jacksonville, FL</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B." last="Calne">Donald B. Calne</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author><author><name sortKey="Wszolek, Zbigniew K" sort="Wszolek, Zbigniew K" uniqKey="Wszolek Z" first="Zbigniew K." last="Wszolek">Zbigniew K. Wszolek</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Mayo Clinic, Jacksonville, FL</wicri:regionArea><placeName><region type="state">Floride</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name><affiliation></affiliation><affiliation><wicri:noCountry code="no comma">Pacific Parkinson's Research Centre and</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2005-12">2005-12</date><biblScope unit="volume">128</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="2777">2777</biblScope><biblScope unit="page" to="2785">2785</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>11C-DTBZ = 11C-(±)α-dihydrotetrabenazine</term><term>11C-MP = 11C-d-threo-methylphenidate</term><term>11C-RAC = 11C-raclopride</term><term>18F-dopa = 18F-6-fluoro-l-dopa</term><term>Adult</term><term>Age Factors</term><term>Aged</term><term>BP = binding potential</term><term>Brain (diagnostic imaging)</term><term>Brain (metabolism)</term><term>Carbon Radioisotopes</term><term>Carboxy-Lyases (metabolism)</term><term>Case-Control Studies</term><term>Comparative study</term><term>Compensation</term><term>DAT = dopamine transporter</term><term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term><term>Emission tomography</term><term>Fluorine Radioisotopes</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>LRRK2 = leucine-rich repeat kinase 2</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Levodopa (metabolism)</term><term>Methylphenidate</term><term>Middle Aged</term><term>Mutation</term><term>Nervous system diseases</term><term>PET = positron emission tomography</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (genetics)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pathophysiology</term><term>Phenotype</term><term>Positron</term><term>Positron emission tomography</term><term>Positron-Emission Tomography</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Radiopharmaceuticals</term><term>Receptors, Dopamine D2 (metabolism)</term><term>Regression Analysis</term><term>Sporadic</term><term>Tetrabenazine (analogs & derivatives)</term><term>Tetrabenazine (metabolism)</term><term>UPDRS = Unified Parkinson's Disease Rating Scale</term><term>VMAT2 = vesicular monoamine transporter</term><term>genetics</term><term>pathophysiology</term><term>positron emission tomography</term><term>sPD = sporadic Parkinson's disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carboxy-Lyases</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Levodopa</term><term>Receptors, Dopamine D2</term><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Carbon Radioisotopes</term><term>Fluorine Radioisotopes</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Methylphenidate</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age Factors</term><term>Aged</term><term>Case-Control Studies</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Middle Aged</term><term>Mutation</term><term>Phenotype</term><term>Positron-Emission Tomography</term><term>Regression Analysis</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Compensation</term><term>Etude comparative</term><term>Mutation</term><term>Parkinson maladie</term><term>Physiopathologie</term><term>Positon</term><term>Sporadique</term><term>Système nerveux pathologie</term><term>Tomographie émission positon</term><term>Tomoscintigraphie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease may arise from multiple aetiologies, including genetic mutations that are for the most part uncommon. We describe here the positron emission tomography (PET) findings in clinically affected and asymptomatic, high-risk members of two autosomal dominantly inherited Parkinson's disease kindreds with recently described mutations at the PARK8 locus, in a novel gene encoding a leucine-rich repeat kinase (LRRK2). Affected family members have l-dopa-responsive parkinsonism with loss of dopaminergic nigral neurons and pleomorphic subcellular pathology. Fifteen family members underwent PET using: 18F-6-fluoro-l-dopa (18F-dopa) to assess dopamine (DA) synthesis and storage, 11C-(±)α-dihydrotetrabenazine (11C-DTBZ) for the vesicular monoamine transporter, and 11C-d-threo-methylphenidate (11C-MP) for the membrane dopamine transporter (DAT). Measurements were compared with normal (n = 33) and sporadic Parkinson's disease (sPD) (n = 67) control groups. Four clinically affected members had findings similar to sPD, with impaired presynaptic DA function affecting the putamen more than the caudate. In two affected members, D2 dopamine receptor binding was intact. Two asymptomatic mutation carriers had abnormal DAT binding with another two developing such abnormalities over 4 years of follow-up. In these individuals, 18F-dopa uptake remained normal, although two of them also displayed abnormal 11C-DTBZ binding. Our study demonstrates that the in vivo neurochemical phenotype of LRRK2 mutations is indistinguishable from that of sPD, despite the pathological heterogeneity of the condition. Furthermore, we suggest that compensatory changes including downregulation of the DAT and upregulation of decarboxylase activity may delay the onset of parkinsonian symptoms.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>États-Unis</li></country><region><li>Floride</li></region></list><tree><noCountry><name sortKey="Adams, John R" sort="Adams, John R" uniqKey="Adams J" first="John R." last="Adams">John R. Adams</name><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B." last="Calne">Donald B. Calne</name><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S." last="Lee">Chong S. Lee</name><name sortKey="Mak, Edwin" sort="Mak, Edwin" uniqKey="Mak E" first="Edwin" last="Mak">Edwin Mak</name><name sortKey="Mckenzie, Jessamyn" sort="Mckenzie, Jessamyn" uniqKey="Mckenzie J" first="Jessamyn" last="Mckenzie">Jessamyn Mckenzie</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J." last="Ruth">Thomas J. Ruth</name><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</name><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name><name sortKey="Van Netten, Hinke" sort="Van Netten, Hinke" uniqKey="Van Netten H" first="Hinke" last="Van Netten">Hinke Van Netten</name></noCountry><country name="États-Unis"><region name="Floride"><name sortKey="Strongosky, Audrey" sort="Strongosky, Audrey" uniqKey="Strongosky A" first="Audrey" last="Strongosky">Audrey Strongosky</name></region><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name><name sortKey="Uitti, Ryan J" sort="Uitti, Ryan J" uniqKey="Uitti R" first="Ryan J." last="Uitti">Ryan J. Uitti</name><name sortKey="Wszolek, Zbigniew K" sort="Wszolek, Zbigniew K" uniqKey="Wszolek Z" first="Zbigniew K." last="Wszolek">Zbigniew K. Wszolek</name></country><country name="Allemagne"><noRegion><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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