Milestones in research on the pathophysiology of Parkinson's disease.
Identifieur interne : 001174 ( PubMed/Curation ); précédent : 001173; suivant : 001175Milestones in research on the pathophysiology of Parkinson's disease.
Auteurs : Thomas Wichmann [États-Unis] ; Mahlon R. Delong ; Jorge Guridi ; Jose A. ObesoSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Basal Ganglia (pathology), Basal Ganglia (physiopathology), Biomedical Research (history), Biomedical Research (methods), History, 20th Century, History, 21st Century, Humans, Neural Pathways (pathology), Neurons (physiology), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- history : Biomedical Research.
- methods : Biomedical Research.
- pathology : Basal Ganglia, Neural Pathways, Parkinson Disease.
- physiology : Neurons.
- physiopathology : Basal Ganglia, Parkinson Disease.
- Animals, History, 20th Century, History, 21st Century, Humans.
Abstract
Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico-subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so-called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation.
DOI: 10.1002/mds.23695
PubMed: 21626548
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Milestones in research on the pathophysiology of Parkinson's disease.</title><author><name sortKey="Wichmann, Thomas" sort="Wichmann, Thomas" uniqKey="Wichmann T" first="Thomas" last="Wichmann">Thomas Wichmann</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA. twichma@emory.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Delong, Mahlon R" sort="Delong, Mahlon R" uniqKey="Delong M" first="Mahlon R" last="Delong">Mahlon R. Delong</name></author><author><name sortKey="Guridi, Jorge" sort="Guridi, Jorge" uniqKey="Guridi J" first="Jorge" last="Guridi">Jorge Guridi</name></author><author><name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="Jose A" last="Obeso">Jose A. Obeso</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="doi">10.1002/mds.23695</idno><idno type="RBID">pubmed:21626548</idno><idno type="pmid">21626548</idno><idno type="wicri:Area/PubMed/Corpus">001174</idno><idno type="wicri:Area/PubMed/Curation">001174</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Milestones in research on the pathophysiology of Parkinson's disease.</title><author><name sortKey="Wichmann, Thomas" sort="Wichmann, Thomas" uniqKey="Wichmann T" first="Thomas" last="Wichmann">Thomas Wichmann</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA. twichma@emory.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Delong, Mahlon R" sort="Delong, Mahlon R" uniqKey="Delong M" first="Mahlon R" last="Delong">Mahlon R. Delong</name></author><author><name sortKey="Guridi, Jorge" sort="Guridi, Jorge" uniqKey="Guridi J" first="Jorge" last="Guridi">Jorge Guridi</name></author><author><name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="Jose A" last="Obeso">Jose A. Obeso</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (physiopathology)</term><term>Biomedical Research (history)</term><term>Biomedical Research (methods)</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term><term>Neural Pathways (pathology)</term><term>Neurons (physiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Biomedical Research</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Biomedical Research</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Neural Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>History, 20th Century</term><term>History, 21st Century</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico-subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so-called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21626548</PMID><DateCreated><Year>2011</Year><Month>05</Month><Day>31</Day></DateCreated><DateCompleted><Year>2011</Year><Month>09</Month><Day>30</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>6</Issue><PubDate><Year>2011</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Milestones in research on the pathophysiology of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1032-41</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23695</ELocationID><Abstract><AbstractText>Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico-subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so-called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation.</AbstractText><CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wichmann</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA. twichma@emory.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DeLong</LastName><ForeName>Mahlon R</ForeName><Initials>MR</Initials></Author><Author ValidYN="Y"><LastName>Guridi</LastName><ForeName>Jorge</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Obeso</LastName><ForeName>Jose 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21st Century</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009434">Neural Pathways</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS650227</OtherID><OtherID Source="NLM">PMC4272856</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23695</ArticleId><ArticleId IdType="pubmed">21626548</ArticleId><ArticleId IdType="pmc">PMC4272856</ArticleId><ArticleId IdType="mid">NIHMS650227</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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