Neuronal vulnerability, pathogenesis and Parkinson’s disease
Identifieur interne : 000C97 ( Main/Exploration ); précédent : 000C96; suivant : 000C98Neuronal vulnerability, pathogenesis and Parkinson’s disease
Auteurs : David Sulzer [États-Unis] ; D. James Surmeier [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2012.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : alpha-Synuclein.
- complications : Nerve Degeneration.
- etiology : Parkinson Disease.
- pathology : Nerve Degeneration, Nervous System, Neurons, Parkinson Disease.
- Humans.
Abstract
Although there have been significant advances, pathogenesis in Parkinson’s disease (PD) is still poorly understood. Potential clues about pathogenesis that have not been systematically pursued are suggested by the restricted pattern of neuronal pathology in the disease. In addition to dopaminergic neurons in the substantia nigra pars compacta (SNc), a significant number of other central and peripheral neuronal populations exhibit Lewy pathology (LP), phenotypic dysregulation or frank degeneration in PD patients. Drawing on this literature, there appears to be a small number of risk factors contributing to vulnerability. These include autonomous activity, broad action potentials, low intrinsic calcium buffering capacity, poorly myelinated long highly branched axons and terminal fields, and use of a monoamine neurotransmitter, often with the catecholamine-derived neuromelanin pigment. Of these phenotypic traits, only the physiological ones appear to provide a reachable therapeutic target at present.
Url:
DOI: 10.1002/mds.25095
PubMed: 22791686
PubMed Central: 3578396
Affiliations:
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Le document en format XML
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James Surmeier</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22791686</idno><idno type="pmc">3578396</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578396</idno><idno type="RBID">PMC:3578396</idno><idno type="doi">10.1002/mds.25095</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000279</idno><idno type="wicri:Area/Pmc/Curation">000279</idno><idno type="wicri:Area/Pmc/Checkpoint">000176</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">000D07</idno><idno type="wicri:Area/PubMed/Curation">000D07</idno><idno type="wicri:Area/PubMed/Checkpoint">000907</idno><idno type="wicri:Area/Ncbi/Merge">003739</idno><idno type="wicri:Area/Ncbi/Curation">003739</idno><idno type="wicri:Area/Ncbi/Checkpoint">003739</idno><idno type="wicri:doubleKey">0885-3185:2012:Sulzer D:neuronal:vulnerability:pathogenesis</idno><idno type="wicri:Area/Main/Merge">000D16</idno><idno type="wicri:Area/Main/Curation">000C97</idno><idno type="wicri:Area/Main/Exploration">000C97</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Neuronal vulnerability, pathogenesis and Parkinson’s disease</title><author><name sortKey="Sulzer, David" sort="Sulzer, David" uniqKey="Sulzer D" first="David" last="Sulzer">David Sulzer</name><affiliation wicri:level="2"><nlm:aff id="A1">Departments of Psychiatry, Neurology & Pharmacology, Columbia University, New York, NY 10032</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Departments of Psychiatry, Neurology & Pharmacology, Columbia University, New York</wicri:cityArea></affiliation></author><author><name sortKey="Surmeier, D James" sort="Surmeier, D James" uniqKey="Surmeier D" first="D. James" last="Surmeier">D. James Surmeier</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago</wicri:cityArea></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans</term><term>Nerve Degeneration (complications)</term><term>Nerve Degeneration (pathology)</term><term>Nervous System (pathology)</term><term>Neurons (pathology)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (pathology)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Nerve Degeneration</term><term>Nervous System</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Although there have been significant advances, pathogenesis in Parkinson’s disease (PD) is still poorly understood. Potential clues about pathogenesis that have not been systematically pursued are suggested by the restricted pattern of neuronal pathology in the disease. In addition to dopaminergic neurons in the substantia nigra pars compacta (SNc), a significant number of other central and peripheral neuronal populations exhibit Lewy pathology (LP), phenotypic dysregulation or frank degeneration in PD patients. Drawing on this literature, there appears to be a small number of risk factors contributing to vulnerability. These include autonomous activity, broad action potentials, low intrinsic calcium buffering capacity, poorly myelinated long highly branched axons and terminal fields, and use of a monoamine neurotransmitter, often with the catecholamine-derived neuromelanin pigment. Of these phenotypic traits, only the physiological ones appear to provide a reachable therapeutic target at present.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Sulzer, David" sort="Sulzer, David" uniqKey="Sulzer D" first="David" last="Sulzer">David Sulzer</name></region><name sortKey="Surmeier, D James" sort="Surmeier, D James" uniqKey="Surmeier D" first="D. James" last="Surmeier">D. James Surmeier</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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