Mitochondrial Abnormalities in the Putamen in Parkinson’s Disease Dyskinesia
Identifieur interne : 000509 ( Main/Exploration ); précédent : 000508; suivant : 000510Mitochondrial Abnormalities in the Putamen in Parkinson’s Disease Dyskinesia
Auteurs : Alipi Naydenov ; Fair Vassoler ; Andrew Luksik ; Joanna Kaczmarska ; Christine KonradiSource :
- Acta neuropathologica [ 0001-6322 ] ; 2010.
Abstract
Prolonged treatment of Parkinson’s disease with levodopa leads to disabling side effects collectively referred to as ‘dyskinesias’. We hypothesized that bioenergetic function in the putamen might play a crucial role in the development of dyskinesias. To test this hypothesis we used post-mortem samples of the human putamen and applied real time-PCR approaches and gene expression microarrays. We found that mitochondrial DNA levels are decreased in patients who have developed dyskinesias, and mitochondrial DNA damage is concomitantly increased. These pathologies were not observed in Parkinson’s disease subjects without signs of dyskinesias. The group of nuclear mRNA transcripts coding for the proteins of the mitochondrial electron transfer chain was decreased in patients with dyskinesias to a larger extent than in patients who had not developed dyskinesias. To examine if dopamine fluctuations affect mitochondrial DNA levels in dopaminoceptive neurons, rat striatal neurons in culture were repeatedly exposed to levodopa, dopamine or their metabolites. Mitochondrial DNA levels were reduced after treatment with dopamine, but not after treatment with dopamine metabolites. Levodopa led to an increase in mitochondrial DNA levels. We conclude that mitochondrial susceptibility in the putamen plays a role in the development of dyskinesias.
Url:
DOI: 10.1007/s00401-010-0740-8
PubMed: 20740286
PubMed Central: 2955799
Affiliations:
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code="subfield">37232</wicri:noCountry></affiliation></author><author><name sortKey="Luksik, Andrew S" sort="Luksik, Andrew S" uniqKey="Luksik A" first="Andrew" last="Luksik">Andrew Luksik</name><affiliation><nlm:aff id="A1">Departments of Pharmacology and Psychiatry, Vanderbilt University, Nashville, Tennessee, 37232</nlm:aff><wicri:noCountry code="subfield">37232</wicri:noCountry></affiliation></author><author><name sortKey="Kaczmarska, Joanna" sort="Kaczmarska, Joanna" uniqKey="Kaczmarska J" first="Joanna" last="Kaczmarska">Joanna Kaczmarska</name><affiliation><nlm:aff id="A1">Departments of Pharmacology and Psychiatry, Vanderbilt University, Nashville, Tennessee, 37232</nlm:aff><wicri:noCountry code="subfield">37232</wicri:noCountry></affiliation></author><author><name sortKey="Konradi, Christine" sort="Konradi, Christine" uniqKey="Konradi C" first="Christine" last="Konradi">Christine Konradi</name><affiliation><nlm:aff id="A1">Departments of Pharmacology and Psychiatry, Vanderbilt University, Nashville, Tennessee, 37232</nlm:aff><wicri:noCountry code="subfield">37232</wicri:noCountry></affiliation><affiliation><nlm:aff id="A2">Center for Molecular Neuroscience, Vanderbilt University, Nashville, Tennessee, 37232</nlm:aff><wicri:noCountry code="subfield">37232</wicri:noCountry></affiliation><affiliation><nlm:aff id="A3">Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee, 37203</nlm:aff><wicri:noCountry code="subfield">37203</wicri:noCountry></affiliation></author></analytic><series><title level="j">Acta neuropathologica</title><idno type="ISSN">0001-6322</idno><idno type="e-ISSN">1432-0533</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Prolonged treatment of Parkinson’s disease with levodopa leads to disabling side effects collectively referred to as ‘dyskinesias’. We hypothesized that bioenergetic function in the putamen might play a crucial role in the development of dyskinesias. To test this hypothesis we used post-mortem samples of the human putamen and applied real time-PCR approaches and gene expression microarrays. We found that mitochondrial DNA levels are decreased in patients who have developed dyskinesias, and mitochondrial DNA damage is concomitantly increased. These pathologies were not observed in Parkinson’s disease subjects without signs of dyskinesias. The group of nuclear mRNA transcripts coding for the proteins of the mitochondrial electron transfer chain was decreased in patients with dyskinesias to a larger extent than in patients who had not developed dyskinesias. To examine if dopamine fluctuations affect mitochondrial DNA levels in dopaminoceptive neurons, rat striatal neurons in culture were repeatedly exposed to levodopa, dopamine or their metabolites. Mitochondrial DNA levels were reduced after treatment with dopamine, but not after treatment with dopamine metabolites. Levodopa led to an increase in mitochondrial DNA levels. We conclude that mitochondrial susceptibility in the putamen plays a role in the development of dyskinesias.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Kaczmarska, Joanna" sort="Kaczmarska, Joanna" uniqKey="Kaczmarska J" first="Joanna" last="Kaczmarska">Joanna Kaczmarska</name><name sortKey="Konradi, Christine" sort="Konradi, Christine" uniqKey="Konradi C" first="Christine" last="Konradi">Christine Konradi</name><name sortKey="Luksik, Andrew S" sort="Luksik, Andrew S" uniqKey="Luksik A" first="Andrew" last="Luksik">Andrew Luksik</name><name sortKey="Naydenov, Alipi V" sort="Naydenov, Alipi V" uniqKey="Naydenov A" first="Alipi" last="Naydenov">Alipi Naydenov</name><name sortKey="Vassoler, Fair" sort="Vassoler, Fair" uniqKey="Vassoler F" first="Fair" last="Vassoler">Fair Vassoler</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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