A multidisciplinary study of patients with early-onset PD with and without parkin mutations.
Identifieur interne : 000B88 ( PubMed/Curation ); précédent : 000B87; suivant : 000B89A multidisciplinary study of patients with early-onset PD with and without parkin mutations.
Auteurs : E. Lohmann [France] ; S. Thobois ; S. Lesage ; E. Broussolle ; S Tezenas Du Montcel ; M-J Ribeiro ; P. Remy ; A. Pelissolo ; B. Dubois ; L. Mallet ; P. Pollak ; Y. Agid ; A. BriceSource :
- Neurology [ 1526-632X ] ; 2009.
English descriptors
- KwdEn :
- Adult, Age of Onset, Aged, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Cognition Disorders (diagnosis), Cognition Disorders (epidemiology), Cognition Disorders (genetics), Comorbidity, DNA Mutational Analysis, Depressive Disorder (diagnosis), Depressive Disorder (epidemiology), Depressive Disorder (genetics), Disease Progression, Drug Resistance (genetics), Female, Genetic Predisposition to Disease (genetics), Genetic Testing, Genotype, Humans, Male, Middle Aged, Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (psychology), Severity of Illness Index, Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , administration & dosage : Antiparkinson Agents.
- chemical , adverse effects : Antiparkinson Agents.
- diagnosis : Cognition Disorders, Depressive Disorder.
- epidemiology : Cognition Disorders, Depressive Disorder, Parkinson Disease.
- genetics : Cognition Disorders, Depressive Disorder, Drug Resistance, Genetic Predisposition to Disease, Parkinson Disease, Ubiquitin-Protein Ligases.
- psychology : Parkinson Disease.
- Adult, Age of Onset, Aged, Comorbidity, DNA Mutational Analysis, Disease Progression, Female, Genetic Testing, Genotype, Humans, Male, Middle Aged, Severity of Illness Index.
Abstract
To establish phenotype-genotype correlations in early-onset Parkinson disease (EOPD), we performed neurologic, neuropsychological, and psychiatric evaluations in a series of patients with and without parkin mutations.
DOI: 10.1212/01.wnl.0000327098.86861.d4
PubMed: 18987353
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pubmed:18987353Le document en format XML
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Lohmann</name><affiliation wicri:level="1"><nlm:affiliation>INSERM UMR S_679, Hôpital Pitié-Salpêtrière, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM UMR S_679, Hôpital Pitié-Salpêtrière, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Thobois, S" sort="Thobois, S" uniqKey="Thobois S" first="S" last="Thobois">S. Thobois</name></author><author><name sortKey="Lesage, S" sort="Lesage, S" uniqKey="Lesage S" first="S" last="Lesage">S. Lesage</name></author><author><name sortKey="Broussolle, E" sort="Broussolle, E" uniqKey="Broussolle E" first="E" last="Broussolle">E. 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Pollak</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name></author></analytic><series><title level="j">Neurology</title><idno type="eISSN">1526-632X</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (epidemiology)</term><term>Cognition Disorders (genetics)</term><term>Comorbidity</term><term>DNA Mutational Analysis</term><term>Depressive Disorder (diagnosis)</term><term>Depressive Disorder (epidemiology)</term><term>Depressive Disorder (genetics)</term><term>Disease Progression</term><term>Drug Resistance (genetics)</term><term>Female</term><term>Genetic Predisposition to Disease (genetics)</term><term>Genetic Testing</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (epidemiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (psychology)</term><term>Severity of Illness Index</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term><term>Depressive Disorder</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Cognition Disorders</term><term>Depressive Disorder</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cognition Disorders</term><term>Depressive Disorder</term><term>Drug Resistance</term><term>Genetic Predisposition to Disease</term><term>Parkinson Disease</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Comorbidity</term><term>DNA Mutational Analysis</term><term>Disease Progression</term><term>Female</term><term>Genetic Testing</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To establish phenotype-genotype correlations in early-onset Parkinson disease (EOPD), we performed neurologic, neuropsychological, and psychiatric evaluations in a series of patients with and without parkin mutations.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18987353</PMID><DateCreated><Year>2009</Year><Month>01</Month><Day>13</Day></DateCreated><DateCompleted><Year>2009</Year><Month>02</Month><Day>20</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1526-632X</ISSN><JournalIssue CitedMedium="Internet"><Volume>72</Volume><Issue>2</Issue><PubDate><Year>2009</Year><Month>Jan</Month><Day>13</Day></PubDate></JournalIssue><Title>Neurology</Title><ISOAbbreviation>Neurology</ISOAbbreviation></Journal><ArticleTitle>A multidisciplinary study of patients with early-onset PD with and without parkin mutations.</ArticleTitle><Pagination><MedlinePgn>110-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1212/01.wnl.0000327098.86861.d4</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To establish phenotype-genotype correlations in early-onset Parkinson disease (EOPD), we performed neurologic, neuropsychological, and psychiatric evaluations in a series of patients with and without parkin mutations.</AbstractText><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Parkin (PARK2) gene mutations are the major cause of autosomal recessive parkinsonism. The usual clinical features are early-onset typical PD with a slow clinical course, an excellent response to low doses of levodopa, frequent treatment-induced dyskinesias, and the absence of dementia.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A total of 44 patients with EOPD (21 with and 23 without parkin mutations) and 9 unaffected single heterozygous carriers of parkin mutations underwent extensive clinical, neuropsychological, and psychiatric examinations.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The neurologic, neuropsychological, and psychiatric features were similar in all patients, except for significantly lower daily doses of dopaminergic treatment and greater delay in the development of levodopa-related fluctuations (p < 0.05) in parkin mutation carriers compared to noncarriers. There was no major difference between the two groups in terms of general cognitive efficiency. Psychiatric manifestations (depression) were more frequent in patients than in healthy single heterozygous parkin carriers but did not differ between the two groups of patients.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Carriers of parkin mutations are clinically indistinguishable from other patients with young-onset Parkinson disease (PD) on an individual basis. Severe generalized loss of dopaminergic neurons in the substantia nigra pars compacta in these patients is associated with an excellent response to low doses of dopa-equivalent and delayed fluctuations, but cognitive impairment and special behavioral or psychiatric symptoms were not more severe than in other patients with early-onset PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lohmann</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>INSERM UMR S_679, Hôpital Pitié-Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thobois</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lesage</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Broussolle</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>du Montcel</LastName><ForeName>S Tezenas</ForeName><Initials>ST</Initials></Author><Author ValidYN="Y"><LastName>Ribeiro</LastName><ForeName>M-J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Remy</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Pelissolo</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Dubois</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Pollak</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><CollectiveName>French Parkinson's Disease Genetics Study Group</CollectiveName></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS41723-01A1</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>11</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurology</MedlineTA><NlmUniqueID>0401060</NlmUniqueID><ISSNLinking>0028-3878</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="C111567">parkin protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 2000 May 25;342(21):1560-7</RefSource><PMID Version="1">10824074</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Med Genet. 2008 Jan;45(1):43-6</RefSource><PMID Version="1">17766365</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Dev. 2000 Sep;22 Suppl 1:S87-91</RefSource><PMID Version="1">10984666</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Mol Life Sci. 2000 Dec;57(13-14):1894-908</RefSource><PMID Version="1">11215516</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2001 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Version="1">18987349</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017668" MajorTopicYN="N">Age of Onset</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="N">Cognition Disorders</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004252" MajorTopicYN="N">DNA Mutational Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003866" MajorTopicYN="N">Depressive Disorder</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004351" MajorTopicYN="N">Drug Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2677494</OtherID><InvestigatorList><Investigator ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Investigator><Investigator ValidYN="Y"><LastName>Bonnet</LastName><ForeName>A-M</ForeName><Initials>AM</Initials></Investigator><Investigator ValidYN="Y"><LastName>Borg</LastName><ForeName>M</ForeName><Initials>M</Initials></Investigator><Investigator ValidYN="Y"><LastName>Brice</LastName><ForeName>A</ForeName><Initials>A</Initials></Investigator><Investigator 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|texte= A multidisciplinary study of patients with early-onset PD with and without parkin mutations.
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Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:18987353" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |