Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: from experimental models to neurodegenerative diseases.
Identifieur interne : 000A80 ( PubMed/Curation ); précédent : 000A79; suivant : 000A81Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: from experimental models to neurodegenerative diseases.
Auteurs : Paolo Gubellini [France] ; Barbara Picconi ; Massimiliano Di Filippo ; Paolo CalabresiSource :
- Biochimica et biophysica acta [ 0006-3002 ] ; 2010.
English descriptors
- KwdEn :
- MESH :
- metabolism : Basal Ganglia, Huntington Disease, Mitochondria, Neurodegenerative Diseases, Parkinson Disease.
- physiopathology : Basal Ganglia.
- Animals, Cell Death, Disease Models, Animal.
Abstract
Mitochondrial dysfunctions have been implicated in the cellular processes underlying several neurodegenerative disorders affecting the basal ganglia. These include Huntington's chorea and Parkinson's disease, two highly debilitating motor disorders for which recent research has also involved gene mutation linked to mitochondrial deficits. Experimental models of basal ganglia diseases have been developed by using toxins able to disrupt mitochondrial function: these molecules act by selectively inhibiting mitochondrial respiratory complexes, uncoupling cellular respiration. This in turn leads to oxidative stress and energy deficit that trigger critical downstream mechanisms, ultimately resulting in neuronal vulnerability and loss. Here we review the molecular and cellular downstream effects triggered by mitochondrial dysfunction, and the different experimental models that are obtained by the administration of selective mitochondrial toxins or by the expression of mutant genes.
DOI: 10.1016/j.bbadis.2009.08.001
PubMed: 19683569
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Here we review the molecular and cellular downstream effects triggered by mitochondrial dysfunction, and the different experimental models that are obtained by the administration of selective mitochondrial toxins or by the expression of mutant genes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19683569</PMID><DateCreated><Year>2009</Year><Month>12</Month><Day>08</Day></DateCreated><DateCompleted><Year>2010</Year><Month>06</Month><Day>16</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>1802</Volume><Issue>1</Issue><PubDate><Year>2010</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Biochimica et biophysica acta</Title><ISOAbbreviation>Biochim. Biophys. 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This in turn leads to oxidative stress and energy deficit that trigger critical downstream mechanisms, ultimately resulting in neuronal vulnerability and loss. Here we review the molecular and cellular downstream effects triggered by mitochondrial dysfunction, and the different experimental models that are obtained by the administration of selective mitochondrial toxins or by the expression of mutant genes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gubellini</LastName><ForeName>Paolo</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Institut de Biologie du Développement de Marseille-Luminy (IBDML), UMR6216 (CNRS/Université de la Méditerranée), Marseille, France. paolo.gubellini@ibdml.univ-mrs.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Picconi</LastName><ForeName>Barbara</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Di Filippo</LastName><ForeName>Massimiliano</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Calabresi</LastName><ForeName>Paolo</ForeName><Initials>P</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><ArticleDate DateType="Electronic"><Year>2009</Year><Month>08</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta</MedlineTA><NlmUniqueID>0217513</NlmUniqueID><ISSNLinking>0006-3002</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006816" MajorTopicYN="N">Huntington Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>192</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>05</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>07</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>08</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>8</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>8</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>6</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19683569</ArticleId><ArticleId IdType="pii">S0925-4439(09)00168-9</ArticleId><ArticleId IdType="doi">10.1016/j.bbadis.2009.08.001</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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