DJ-1, PINK1 and their effects on Mitochondrial Pathways
Identifieur interne : 000355 ( Pmc/Checkpoint ); précédent : 000354; suivant : 000356DJ-1, PINK1 and their effects on Mitochondrial Pathways
Auteurs : Mark R. CooksonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2010.
Abstract
Genetic forms of parkinsonism are interesting for two particular reasons. First, finding a gene identifies a cause for a disease that would otherwise be unexplained. Second, finding several genes for the same disorder allows us to reconstruct molecular pathways that, in the example of Parkinson’s disease, are be associated with the survival of dopamine neurons in the substantia nigra. Two rare causes of parkinsonism, DJ-1 and PINK1, are associated with mitochondria. This organelle has long been linked with Parkinson’s disease, and recent results are starting to show how mutations impact mitochondrial function. In this short review, I will discuss how we can use some of this information to understand why it is that neurons become dysfunctional in PD.
Url:
DOI: 10.1002/mds.22713
PubMed: 20187230
PubMed Central: 2840196
Affiliations:
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<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8610688</journal-id><journal-id journal-id-type="pubmed-jr-id">5937</journal-id><journal-id journal-id-type="nlm-ta">Mov Disord</journal-id><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20187230</article-id><article-id pub-id-type="pmc">2840196</article-id><article-id pub-id-type="doi">10.1002/mds.22713</article-id><article-id pub-id-type="manuscript">NIHMS146199</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>DJ-1, PINK1 and their effects on Mitochondrial Pathways</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Cookson</surname><given-names>Mark R</given-names></name><degrees>Ph.D</degrees><aff id="A1">Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, NIH. Building 35, Room 1A116, MSC 3707, 35 Convent Drive, Bethesda, MD 20982-3707. Tel 1 301 451 3870; Fax 1 301 480 0315;<email>cookson@mail.nih.gov</email></aff></contrib></contrib-group><pub-date pub-type="nihms-submitted"><day>17</day><month>9</month><year>2009</year></pub-date><pub-date pub-type="ppub"><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>1</month><year>2011</year></pub-date><volume>25</volume><issue>Suppl 1</issue><fpage>S44</fpage><lpage>S48</lpage><abstract><p id="P1">Genetic forms of parkinsonism are interesting for two particular reasons. First, finding a gene identifies a cause for a disease that would otherwise be unexplained. Second, finding several genes for the same disorder allows us to reconstruct molecular pathways that, in the example of Parkinson’s disease, are be associated with the survival of dopamine neurons in the substantia nigra. Two rare causes of parkinsonism, DJ-1 and PINK1, are associated with mitochondria. This organelle has long been linked with Parkinson’s disease, and recent results are starting to show how mutations impact mitochondrial function. In this short review, I will discuss how we can use some of this information to understand why it is that neurons become dysfunctional in PD.</p></abstract><contract-num rid="AG1">Z01 AG000940-01
||AG</contract-num><contract-sponsor id="AG1">National Institute on Aging : NIA</contract-sponsor></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Cookson, Mark R" sort="Cookson, Mark R" uniqKey="Cookson M" first="Mark R" last="Cookson">Mark R. Cookson</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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