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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">PGC-1α at the intersection of bioenergetics regulation and neuron function: From Huntington’s disease to Parkinson’s disease and beyond</title><author><name sortKey="Tsunemi, Taiji" sort="Tsunemi, Taiji" uniqKey="Tsunemi T" first="Taiji" last="Tsunemi">Taiji Tsunemi</name><affiliation><nlm:aff id="A1">Department of Pediatrics, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation></author><author><name sortKey="La Spada, Albert R" sort="La Spada, Albert R" uniqKey="La Spada A" first="Albert R." last="La Spada">Albert R. La Spada</name><affiliation><nlm:aff id="A1">Department of Pediatrics, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Cellular & Molecular Medicine, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Division of Biological Sciences, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Institute for Genomic Medicine, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Rady Children’s Hospital, San Diego, CA 92123, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22100502</idno><idno type="pmc">3506171</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506171</idno><idno type="RBID">PMC:3506171</idno><idno type="doi">10.1016/j.pneurobio.2011.10.004</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000243</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000243</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">PGC-1α at the intersection of bioenergetics regulation and neuron function: From Huntington’s disease to Parkinson’s disease and beyond</title><author><name sortKey="Tsunemi, Taiji" sort="Tsunemi, Taiji" uniqKey="Tsunemi T" first="Taiji" last="Tsunemi">Taiji Tsunemi</name><affiliation><nlm:aff id="A1">Department of Pediatrics, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation></author><author><name sortKey="La Spada, Albert R" sort="La Spada, Albert R" uniqKey="La Spada A" first="Albert R." last="La Spada">Albert R. La Spada</name><affiliation><nlm:aff id="A1">Department of Pediatrics, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Department of Cellular & Molecular Medicine, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Division of Biological Sciences, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Institute for Genomic Medicine, University of California, San Diego; La Jolla, CA 92093, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Rady Children’s Hospital, San Diego, CA 92123, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Progress in neurobiology</title><idno type="ISSN">0301-0082</idno><idno type="eISSN">1873-5118</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Neurons are specialized cells with unique features, including a constant high demand for energy. Mitochondria satisfy this constant demand, and are emerging as a central target for dysfunction in neurodegenerative disorders, such as Huntington’s disease (HD) and Parkinson’s disease. PPARγ co-activator-1α (PGC-1α) is a transcription co-activator for nuclear receptors such as the PPARs, and thereby coordinates a number of gene expression programs to promote mitochondrial biogenesis and oxidative phosphorylation. Studies of PGC-1α knock-out mice have yielded important insights into the role of PGC-1α in normal nervous system function and potentially neurological disease. HD is caused by a polyglutamine repeat expansion in the huntingtin protein, and decades of work have established mitochondrial dysfunction as a key feature of HD pathogenesis. However, after the discovery of the HD gene, numerous reports produced strong evidence for altered transcription in HD. In 2006, a series of studies revealed that PGC-1α transcription interference contributes to HD neurodegeneration, linking the nuclear transcriptionopathy with the mitochondrial dysfunction. Subsequent work has strengthened this view, and further extended the role of PGC-1α within the CNS. Within the last year, studies of Parkinson’s disease, another involuntary movement disorder long associated with mitochondrial dysfunction, have shown that PGC-1α dysregulation is contributing to its pathogenesis. As PGC-1α is likely also important for aging, a process with considerable relevance to neuron function, translational studies aimed at developing therapies based upon the PGC-1α pathway as a high priority target are underway.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0370121</journal-id><journal-id journal-id-type="pubmed-jr-id">6712</journal-id><journal-id journal-id-type="nlm-ta">Prog Neurobiol</journal-id><journal-id journal-id-type="iso-abbrev">Prog. Neurobiol.</journal-id><journal-title-group><journal-title>Progress in neurobiology</journal-title></journal-title-group><issn pub-type="ppub">0301-0082</issn><issn pub-type="epub">1873-5118</issn></journal-meta><article-meta><article-id pub-id-type="pmid">22100502</article-id><article-id pub-id-type="pmc">3506171</article-id><article-id pub-id-type="doi">10.1016/j.pneurobio.2011.10.004</article-id><article-id pub-id-type="manuscript">NIHMS416953</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>PGC-1α at the intersection of bioenergetics regulation and neuron function: From Huntington’s disease to Parkinson’s disease and beyond</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Tsunemi</surname><given-names>Taiji</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>La Spada</surname><given-names>Albert R.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref><xref ref-type="aff" rid="A4">4</xref><xref ref-type="aff" rid="A5">5</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Pediatrics, University of California, San Diego; La Jolla, CA 92093, USA</aff><aff id="A2"><label>2</label>Department of Cellular & Molecular Medicine, University of California, San Diego; La Jolla, CA 92093, USA</aff><aff id="A3"><label>3</label>Division of Biological Sciences, University of California, San Diego; La Jolla, CA 92093, USA</aff><aff id="A4"><label>4</label>Institute for Genomic Medicine, University of California, San Diego; La Jolla, CA 92093, USA</aff><aff id="A5"><label>5</label>Rady Children’s Hospital, San Diego, CA 92123, USA</aff><author-notes><corresp id="cor1">Corresponding author: Albert La Spada, MD, PhD, Pediatrics and Cellular & Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, MC 0642, La Jolla, CA 92093-0642, (858)-246-0148 [ph.], <email>alaspada@ucsd.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>26</day><month>10</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>09</day><month>11</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>5</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>26</day><month>11</month><year>2012</year></pub-date><volume>97</volume><issue>2</issue><fpage>142</fpage><lpage>151</lpage><abstract><p id="P1">Neurons are specialized cells with unique features, including a constant high demand for energy. Mitochondria satisfy this constant demand, and are emerging as a central target for dysfunction in neurodegenerative disorders, such as Huntington’s disease (HD) and Parkinson’s disease. PPARγ co-activator-1α (PGC-1α) is a transcription co-activator for nuclear receptors such as the PPARs, and thereby coordinates a number of gene expression programs to promote mitochondrial biogenesis and oxidative phosphorylation. Studies of PGC-1α knock-out mice have yielded important insights into the role of PGC-1α in normal nervous system function and potentially neurological disease. HD is caused by a polyglutamine repeat expansion in the huntingtin protein, and decades of work have established mitochondrial dysfunction as a key feature of HD pathogenesis. However, after the discovery of the HD gene, numerous reports produced strong evidence for altered transcription in HD. In 2006, a series of studies revealed that PGC-1α transcription interference contributes to HD neurodegeneration, linking the nuclear transcriptionopathy with the mitochondrial dysfunction. Subsequent work has strengthened this view, and further extended the role of PGC-1α within the CNS. Within the last year, studies of Parkinson’s disease, another involuntary movement disorder long associated with mitochondrial dysfunction, have shown that PGC-1α dysregulation is contributing to its pathogenesis. As PGC-1α is likely also important for aging, a process with considerable relevance to neuron function, translational studies aimed at developing therapies based upon the PGC-1α pathway as a high priority target are underway.</p></abstract><funding-group><award-group><funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source><award-id>R01 NS065874 || NS</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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