Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.
Identifieur interne : 001B18 ( PubMed/Curation ); précédent : 001B17; suivant : 001B19Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.
Auteurs : Bart F L. Van Nuenen [Pays-Bas] ; Thilo Van Eimeren ; Joyce P M. Van Der Vegt ; Carsten Buhmann ; Christine Klein ; Bastiaan R. Bloem ; Hartwig R. SiebnerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Fingers (physiology), Genomics (methods), Humans, Magnetic Resonance Imaging, Movement (physiology), Mutation (physiology), Parkinson Disease (diagnosis), Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Protein Kinases (genetics), Psychomotor Performance (physiology), Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Protein Kinases, Ubiquitin-Protein Ligases.
- chemical , therapeutic use : Antiparkinson Agents.
- diagnosis : Parkinson Disease.
- drug therapy : Parkinson Disease.
- genetics : Parkinson Disease.
- methods : Genomics.
- physiology : Fingers, Movement, Mutation, Psychomotor Performance.
- physiopathology : Parkinson Disease.
- Humans, Magnetic Resonance Imaging.
Abstract
Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non-manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how "generically" the human brain compensates for a preclinical dopaminergic dysfunction.
DOI: 10.1002/mds.22635
PubMed: 19877238
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :001B18
Links to Exploration step
pubmed:19877238Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.</title><author><name sortKey="Van Nuenen, Bart F L" sort="Van Nuenen, Bart F L" uniqKey="Van Nuenen B" first="Bart F L" last="Van Nuenen">Bart F L. Van Nuenen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen</wicri:regionArea></affiliation></author><author><name sortKey="Van Eimeren, Thilo" sort="Van Eimeren, Thilo" uniqKey="Van Eimeren T" first="Thilo" last="Van Eimeren">Thilo Van Eimeren</name></author><author><name sortKey="Van Der Vegt, Joyce P M" sort="Van Der Vegt, Joyce P M" uniqKey="Van Der Vegt J" first="Joyce P M" last="Van Der Vegt">Joyce P M. Van Der Vegt</name></author><author><name sortKey="Buhmann, Carsten" sort="Buhmann, Carsten" uniqKey="Buhmann C" first="Carsten" last="Buhmann">Carsten Buhmann</name></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R" last="Bloem">Bastiaan R. Bloem</name></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R" last="Siebner">Hartwig R. Siebner</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="doi">10.1002/mds.22635</idno><idno type="RBID">pubmed:19877238</idno><idno type="pmid">19877238</idno><idno type="wicri:Area/PubMed/Corpus">001B18</idno><idno type="wicri:Area/PubMed/Curation">001B18</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.</title><author><name sortKey="Van Nuenen, Bart F L" sort="Van Nuenen, Bart F L" uniqKey="Van Nuenen B" first="Bart F L" last="Van Nuenen">Bart F L. Van Nuenen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen</wicri:regionArea></affiliation></author><author><name sortKey="Van Eimeren, Thilo" sort="Van Eimeren, Thilo" uniqKey="Van Eimeren T" first="Thilo" last="Van Eimeren">Thilo Van Eimeren</name></author><author><name sortKey="Van Der Vegt, Joyce P M" sort="Van Der Vegt, Joyce P M" uniqKey="Van Der Vegt J" first="Joyce P M" last="Van Der Vegt">Joyce P M. Van Der Vegt</name></author><author><name sortKey="Buhmann, Carsten" sort="Buhmann, Carsten" uniqKey="Buhmann C" first="Carsten" last="Buhmann">Carsten Buhmann</name></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R" last="Bloem">Bastiaan R. Bloem</name></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R" last="Siebner">Hartwig R. Siebner</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="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term><term>Fingers (physiology)</term><term>Genomics (methods)</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Movement (physiology)</term><term>Mutation (physiology)</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Protein Kinases (genetics)</term><term>Psychomotor Performance (physiology)</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein Kinases</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Genomics</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Fingers</term><term>Movement</term><term>Mutation</term><term>Psychomotor Performance</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>Magnetic Resonance Imaging</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non-manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how "generically" the human brain compensates for a preclinical dopaminergic dysfunction.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19877238</PMID><DateCreated><Year>2009</Year><Month>11</Month><Day>05</Day></DateCreated><DateCompleted><Year>2010</Year><Month>01</Month><Day>26</Day></DateCompleted><DateRevised><Year>2012</Year><Month>06</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>24 Suppl 2</Volume><PubDate><Year>2009</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.</ArticleTitle><Pagination><MedlinePgn>S703-10</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22635</ELocationID><Abstract><AbstractText>Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non-manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how "generically" the human brain compensates for a preclinical dopaminergic dysfunction.</AbstractText><CopyrightInformation>Copyright 2009 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>van Nuenen</LastName><ForeName>Bart F L</ForeName><Initials>BF</Initials><AffiliationInfo><Affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Eimeren</LastName><ForeName>Thilo</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>van der Vegt</LastName><ForeName>Joyce P M</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Buhmann</LastName><ForeName>Carsten</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Klein</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Bloem</LastName><ForeName>Bastiaan R</ForeName><Initials>BR</Initials></Author><Author ValidYN="Y"><LastName>Siebner</LastName><ForeName>Hartwig R</ForeName><Initials>HR</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.-</RegistryNumber><NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C433927">PTEN-induced putative kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 6.3.2.19</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 6.3.2.19</RegistryNumber><NameOfSubstance UI="C111567">parkin protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005385">Fingers</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D023281">Genomics</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008279">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009068">Movement</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009154">Mutation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011494">Protein Kinases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011597">Psychomotor Performance</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D044767">Ubiquitin-Protein Ligases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>43</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>1</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.22635</ArticleId><ArticleId IdType="pubmed">19877238</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001B18 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 001B18 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:19877238
|texte= Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:19877238" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a MovDisordV3
| This area was generated with Dilib version V0.6.23. |  |