Parkinson's disease: A broken nosology
Identifieur interne : 003802 ( Main/Exploration ); précédent : 003801; suivant : 003803Parkinson's disease: A broken nosology
Auteurs : John Hardy [États-Unis, Royaume-Uni] ; Andrew Lees (neurologue) [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Humans, Lewy Bodies (pathology), Lewy body dementia, Nerve Tissue Proteins (genetics), Nervous system diseases, Nosology, Nuclear Proteins, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Repressor Proteins, Substantia Nigra (pathology), Ubiquitin-Protein Ligases (genetics), alpha-Synuclein (genetics), nosology.
- 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 α‐synuclein gene. However, the phenotype of this one known cause is broader than PD and encompasses Lewy body dementia. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20532
Affiliations:
- Royaume-Uni, États-Unis
- Angleterre, Grand Londres, Maryland
- Londres
- National Hospital for Neurology and Neurosurgery
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Le document en format XML
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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="2005-08">2005-08</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">S12</biblScope><biblScope unit="supplement">S12</biblScope><biblScope unit="page" from="S2">S2</biblScope><biblScope unit="page" to="S4">S4</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CA96636F5695870FA1BB2E88BE4265E3CE5BDC3A</idno><idno type="DOI">10.1002/mds.20532</idno><idno type="ArticleID">MDS20532</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans</term><term>Lewy Bodies (pathology)</term><term>Lewy body dementia</term><term>Nerve Tissue Proteins (genetics)</term><term>Nervous system diseases</term><term>Nosology</term><term>Nuclear Proteins</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Repressor Proteins</term><term>Substantia Nigra (pathology)</term><term>Ubiquitin-Protein Ligases (genetics)</term><term>alpha-Synuclein (genetics)</term><term>nosology</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></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Nuclear Proteins</term><term>Repressor Proteins</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Démence corps Lewy</term><term>Nosologie</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><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 α‐synuclein gene. However, the phenotype of this one known cause is broader than PD and encompasses Lewy body dementia. © 2005 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>Maryland</li></region><settlement><li>Londres</li></settlement><orgName><li>National Hospital for Neurology and Neurosurgery</li></orgName></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name></region></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Hardy, John" sort="Hardy, John" uniqKey="Hardy J" first="John" last="Hardy">John Hardy</name></region><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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