Parkinson's disease: a broken nosology.
Identifieur interne : 001369 ( Ncbi/Curation ); précédent : 001368; suivant : 001370Parkinson's disease: a broken nosology.
Auteurs : John Hardy [États-Unis] ; Andrew J. LeesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Nerve Tissue Proteins, Ubiquitin-Protein Ligases, alpha-Synuclein.
- genetics : Parkinson Disease.
- pathology : Lewy Bodies, Parkinson Disease, Substantia Nigra.
- physiopathology : Parkinson Disease.
- Humans, Nuclear Proteins, Repressor Proteins.
Abstract
Parkinson's disease (PD) is a clinical diagnosis. We argue here that if we are to make progress in understanding its underlying pathogenesis, there is a need to have a pathological definition of disease that includes the presence of Lewy bodies and nigral loss in the ventrolateral tier of the pars compacta of the substantia nigra. Using such a definition, there is only one certain and known cause: mutations in the alpha-synuclein gene. However, the phenotype of this one known cause is broader than PD and encompasses Lewy body dementia.
DOI: 10.1002/mds.20532
PubMed: 16092073
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pubmed:16092073Le document en format XML
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<author><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name>
<affiliation wicri:level="2"><nlm:affiliation>Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. hardyj@mail.nih.gov</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
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<author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J" last="Lees">Andrew J. Lees</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Parkinson's disease: a broken nosology.</title>
<author><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name>
<affiliation wicri:level="2"><nlm:affiliation>Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. hardyj@mail.nih.gov</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
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<author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J" last="Lees">Andrew J. Lees</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<imprint><date when="2005" type="published">2005</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans</term>
<term>Lewy Bodies (pathology)</term>
<term>Nerve Tissue Proteins (genetics)</term>
<term>Nuclear Proteins</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Repressor Proteins</term>
<term>Substantia Nigra (pathology)</term>
<term>Ubiquitin-Protein Ligases (genetics)</term>
<term>alpha-Synuclein (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term>
<term>Ubiquitin-Protein Ligases</term>
<term>alpha-Synuclein</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lewy Bodies</term>
<term>Parkinson Disease</term>
<term>Substantia Nigra</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
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<term>Repressor Proteins</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a clinical diagnosis. We argue here that if we are to make progress in understanding its underlying pathogenesis, there is a need to have a pathological definition of disease that includes the presence of Lewy bodies and nigral loss in the ventrolateral tier of the pars compacta of the substantia nigra. Using such a definition, there is only one certain and known cause: mutations in the alpha-synuclein gene. However, the phenotype of this one known cause is broader than PD and encompasses Lewy body dementia.</div>
</front>
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