MovDisordV3, Main, Exploration, bibRecord, 002184

Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F‐dopa PET progression study

Identifieur interne : 002184 ( Main/Exploration ); précédent : 002183; suivant : 002185

Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F‐dopa PET progression study

Auteurs : Nicola Pavese [Royaume-Uni] ; Naheed L. Khan [Royaume-Uni] ; Christoph Scherfler [Royaume-Uni] ; Lisa Cohen [Royaume-Uni] ; David J. Brooks [Royaume-Uni] ; Nicholas W. Wood [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni] ; Niall P. Quinn [Royaume-Uni] ; Andrew Lees (neurologue) [Royaume-Uni] ; Paola Piccini [Royaume-Uni]

Source :

Movement Disorders [ 0885-3185 ] ; 2009-11-15.

RBID : ISTEX:5E4E3214B288CEBD88AB8EA901E95679901D6E03

Descripteurs français

Pascal (Inist)
- Dopa, Homozygotie, Maladie de Parkinson, Parkine, Pathologie du système nerveux, Porteur, Tomographie par émission de positons, Tomoscintigraphie, Trouble fonctionnel.

English descriptors

KwdEn :
- 18F‐dopa, Aged, Carrier, Corpus Striatum (pathology), Corpus Striatum (physiopathology), Corpus Striatum (radionuclide imaging), Dihydroxyphenylalanine (analogs & derivatives), Dihydroxyphenylalanine (diagnostic use), Dihydroxyphenylalanine (drug effects), Dopa, Dysfunction, Emission tomography, Female, Heterozygote, Homozygosity, Humans, Longitudinal Studies, Male, Middle Aged, Nervous system diseases, PET, Parkin, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Parkinson disease, Parkinson's disease, Positron emission tomography, Positron-Emission Tomography (methods), Substantia Nigra (pathology), Substantia Nigra (physiopathology), Substantia Nigra (radionuclide imaging), Ubiquitin-Protein Ligases (genetics), parkin, progression.
MESH :
- chemical , analogs & derivatives : Dihydroxyphenylalanine.
- chemical , diagnostic use : Dihydroxyphenylalanine.
- chemical , drug effects : Dihydroxyphenylalanine.
- genetics : Parkinson Disease, Ubiquitin-Protein Ligases.
- methods : Positron-Emission Tomography.
- pathology : Corpus Striatum, Parkinson Disease, Substantia Nigra.
- physiopathology : Corpus Striatum, Substantia Nigra.
- radionuclide imaging : Corpus Striatum, Parkinson Disease, Substantia Nigra.
- Aged, Female, Heterozygote, Humans, Longitudinal Studies, Male, Middle Aged.

Abstract

Little is known about the rate of progression of striatal dysfunction in subjects with parkin‐linked parkinsonism. Being a heterozygous parkin gene carrier may confer susceptibility to Parkinson's disease (PD). In a previous 18F‐dopa PET study, we reported that 69% of carriers of a single parkin mutation showed subclinical loss of putamen dopaminergic function. Using serial 18F‐dopa PET, the present longitudinal study addresses rates of progression of nigrostriatal dysfunction in both compound heterozygous (parkin‐linked parkinsonism) and single heterozygous parkin gene carriers. Three symptomatic patients who were compound heterozygotes for parkin gene mutations and six asymptomatic heterozygous carriers were clinically assessed and had 18F‐dopa PET at baseline and again after 5 years. The patients with symptomatic parkin showed a mean 0.5% annual reduction in putamen 18F‐dopa uptake over 5 years while caudate 18F‐dopa uptake declined by a mean annual rate of 2 %. The asymptomatic heterozygote gene carriers showed a mean 0.56% annual reduction in putamen and 0.62 % annual reduction in caudate 18F‐dopa uptake. Neurological examination at both baseline and follow‐up showed no evidence of parkinsonism. Loss of nigrostriatal dysfunction in parkin‐linked parkinsonism occurs at a very slow rate compared to the 9–12% annual loss of putamen 18F‐dopa uptake reported for idiopathic PD. Although subclinical reductions of striatal 18F‐dopa uptake are common in carriers of a single parkin mutation their slow rate of progression suggests that few if any of these will develop clinical parkinsonism. © 2009 Movement Disorder Society

Url:

https://api.istex.fr/document/5E4E3214B288CEBD88AB8EA901E95679901D6E03/fulltext/pdf

DOI: 10.1002/mds.22817

Affiliations:

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>18F‐dopa</term>
<term>Aged</term>
<term>Carrier</term>
<term>Corpus Striatum (pathology)</term>
<term>Corpus Striatum (physiopathology)</term>
<term>Corpus Striatum (radionuclide imaging)</term>
<term>Dihydroxyphenylalanine (analogs & derivatives)</term>
<term>Dihydroxyphenylalanine (diagnostic use)</term>
<term>Dihydroxyphenylalanine (drug effects)</term>
<term>Dopa</term>
<term>Dysfunction</term>
<term>Emission tomography</term>
<term>Female</term>
<term>Heterozygote</term>
<term>Homozygosity</term>
<term>Humans</term>
<term>Longitudinal Studies</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Nervous system diseases</term>
<term>PET</term>
<term>Parkin</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (radionuclide imaging)</term>
<term>Parkinson disease</term>
<term>Parkinson's disease</term>
<term>Positron emission tomography</term>
<term>Positron-Emission Tomography (methods)</term>
<term>Substantia Nigra (pathology)</term>
<term>Substantia Nigra (physiopathology)</term>
<term>Substantia Nigra (radionuclide imaging)</term>
<term>Ubiquitin-Protein Ligases (genetics)</term>
<term>parkin</term>
<term>progression</term>
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<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Dihydroxyphenylalanine</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term>
<term>Ubiquitin-Protein Ligases</term>
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<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term>
<term>Parkinson Disease</term>
<term>Substantia Nigra</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Dopa</term>
<term>Homozygotie</term>
<term>Maladie de Parkinson</term>
<term>Parkine</term>
<term>Pathologie du   système nerveux</term>
<term>Porteur</term>
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<front><div type="abstract" xml:lang="en">Little is known about the rate of progression of striatal dysfunction in subjects with parkin‐linked parkinsonism. Being a heterozygous parkin gene carrier may confer susceptibility to Parkinson's disease (PD). In a previous 18F‐dopa PET study, we reported that 69% of carriers of a single parkin mutation showed subclinical loss of putamen dopaminergic function. Using serial 18F‐dopa PET, the present longitudinal study addresses rates of progression of nigrostriatal dysfunction in both compound heterozygous (parkin‐linked parkinsonism) and single heterozygous parkin gene carriers. Three symptomatic patients who were compound heterozygotes for parkin gene mutations and six asymptomatic heterozygous carriers were clinically assessed and had 18F‐dopa PET at baseline and again after 5 years. The patients with symptomatic parkin showed a mean 0.5% annual reduction in putamen 18F‐dopa uptake over 5 years while caudate 18F‐dopa uptake declined by a mean annual rate of 2 %. The asymptomatic heterozygote gene carriers showed a mean 0.56% annual reduction in putamen and 0.62 % annual reduction in caudate 18F‐dopa uptake. Neurological examination at both baseline and follow‐up showed no evidence of parkinsonism. Loss of nigrostriatal dysfunction in parkin‐linked parkinsonism occurs at a very slow rate compared to the 9–12% annual loss of putamen 18F‐dopa uptake reported for idiopathic PD. Although subclinical reductions of striatal 18F‐dopa uptake are common in carriers of a single parkin mutation their slow rate of progression suggests that few if any of these will develop clinical parkinsonism. © 2009 Movement Disorder Society</div>
</front>
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<li>Grand Londres</li>
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<name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name>
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<name sortKey="Cohen, Lisa" sort="Cohen, Lisa" uniqKey="Cohen L" first="Lisa" last="Cohen">Lisa Cohen</name>
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<name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name>
<name sortKey="Pavese, Nicola" sort="Pavese, Nicola" uniqKey="Pavese N" first="Nicola" last="Pavese">Nicola Pavese</name>
<name sortKey="Piccini, Paola" sort="Piccini, Paola" uniqKey="Piccini P" first="Paola" last="Piccini">Paola Piccini</name>
<name sortKey="Piccini, Paola" sort="Piccini, Paola" uniqKey="Piccini P" first="Paola" last="Piccini">Paola Piccini</name>
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   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:5E4E3214B288CEBD88AB8EA901E95679901D6E03
   |texte=   Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F‐dopa PET progression study
}}

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Movement Disorders (revue)

Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F‐dopa PET progression study

Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F‐dopa PET progression study

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	Movement Disorders (revue)
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