[Parkinson's disease: new explanatory concepts focused on the cellular mechanisms].
Identifieur interne : 000743 ( PubMed/Corpus ); précédent : 000742; suivant : 000744[Parkinson's disease: new explanatory concepts focused on the cellular mechanisms].
Auteurs : David GrabliSource :
- La Revue du praticien [ 0035-2640 ] ; 2013.
English descriptors
- KwdEn :
- Aged, Cell Physiological Phenomena (genetics), Concept Formation, Female, Gene-Environment Interaction, Humans, Models, Biological, Neurons (metabolism), Neurons (physiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson Disease (therapy), Signal Transduction (genetics), Signal Transduction (physiology).
- MESH :
- etiology : Parkinson Disease.
- genetics : Cell Physiological Phenomena, Parkinson Disease, Signal Transduction.
- metabolism : Neurons.
- physiology : Neurons, Signal Transduction.
- therapy : Parkinson Disease.
- Aged, Concept Formation, Female, Gene-Environment Interaction, Humans, Models, Biological.
Abstract
Parkinson's disease is a neurodegenerative disorder characterized by a cardinal clinical triad that comprises resting tremor, akinesia and plastic hypertonia. The main lesion is a loss of midbbrain dopaminergic neurons but throughout the disease evolution, other neuronal systems will also degenerate. Starting from a typical clinical vignette, this review aims at illustrating how neurosciences helped to shape our knowledge of Parkinson's disease mechanisms at two complementary levels: first regarding the cellular dysfunctions leading to neuronal death and second regarding the neuronal networks involved in the occurrence of motor and non-motor symptoms. The paradigmatic example of subthalamic nucleus deep brain stimulation that dramatically transformed the treatment of patients with advanced Parkinson disease illustrates why the dialog between fundamental and clinical neurosciences is crucial for therapeutic advances.
PubMed: 23789487
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pubmed:23789487Le document en format XML
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The main lesion is a loss of midbbrain dopaminergic neurons but throughout the disease evolution, other neuronal systems will also degenerate. Starting from a typical clinical vignette, this review aims at illustrating how neurosciences helped to shape our knowledge of Parkinson's disease mechanisms at two complementary levels: first regarding the cellular dysfunctions leading to neuronal death and second regarding the neuronal networks involved in the occurrence of motor and non-motor symptoms. The paradigmatic example of subthalamic nucleus deep brain stimulation that dramatically transformed the treatment of patients with advanced Parkinson disease illustrates why the dialog between fundamental and clinical neurosciences is crucial for therapeutic advances.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23789487</PMID><DateCreated><Year>2013</Year><Month>06</Month><Day>24</Day></DateCreated><DateCompleted><Year>2013</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>06</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0035-2640</ISSN><JournalIssue CitedMedium="Print"><Volume>63</Volume><Issue>5</Issue><PubDate><Year>2013</Year><Month>May</Month></PubDate></JournalIssue><Title>La Revue du praticien</Title><ISOAbbreviation>Rev Prat</ISOAbbreviation></Journal><ArticleTitle>[Parkinson's disease: new explanatory concepts focused on the cellular mechanisms].</ArticleTitle><Pagination><MedlinePgn>634-8</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease is a neurodegenerative disorder characterized by a cardinal clinical triad that comprises resting tremor, akinesia and plastic hypertonia. The main lesion is a loss of midbbrain dopaminergic neurons but throughout the disease evolution, other neuronal systems will also degenerate. Starting from a typical clinical vignette, this review aims at illustrating how neurosciences helped to shape our knowledge of Parkinson's disease mechanisms at two complementary levels: first regarding the cellular dysfunctions leading to neuronal death and second regarding the neuronal networks involved in the occurrence of motor and non-motor symptoms. The paradigmatic example of subthalamic nucleus deep brain stimulation that dramatically transformed the treatment of patients with advanced Parkinson disease illustrates why the dialog between fundamental and clinical neurosciences is crucial for therapeutic advances.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Grabli</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Département de neurologie, groupe hospitalier La Pitié-Salpêtrière, AP-HP, 75013 Paris, France. david.grabli@psl.aphp.fr</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Maladie de parkinson: de nouveaux concepts explicatifs centrés sur les mécanismes cellulaires.</VernacularTitle></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Rev Prat</MedlineTA><NlmUniqueID>0404334</NlmUniqueID><ISSNLinking>0035-2640</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002468" MajorTopicYN="Y">Cell Physiological Phenomena</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003210" MajorTopicYN="N">Concept Formation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059647" MajorTopicYN="N">Gene-Environment Interaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>6</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>6</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23789487</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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