{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:08:05Z","timestamp":1789949285632,"version":"4.0.1"},"reference-count":40,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Mol Neurodegeneration"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Huntington disease (HD) is an inherited neurodegenerative disease caused by an abnormal expansion of a CAG repeat in the huntingtin <jats:italic>HTT<\/jats:italic> (<jats:italic>HD<\/jats:italic>) gene. The primary genetic determinant of the age at onset (AO) is the length of the <jats:italic>HTT<\/jats:italic> CAG repeat; however, the remaining genetic contribution to the AO of HD has largely not been elucidated. Recent studies showed that impaired functioning of the peroxisome proliferator-activated receptor <jats:italic>gamma<\/jats:italic> coactivator 1a (PGC-1<jats:italic>alpha<\/jats:italic>) contributes to mitochondrial dysfunction and appears to play an important role in HD pathogenesis. Further genetic evidence for involvement of PGC-1<jats:italic>alpha<\/jats:italic> in HD pathogenesis was generated by the findings that sequence variations in the <jats:italic>PPARGC1A<\/jats:italic> gene encoding PGC-1<jats:italic>alpha<\/jats:italic> exert modifying effects on the AO in HD. In this study, we hypothesised that polymorphisms in PGC-1<jats:italic>alpha<\/jats:italic> downstream targets might also contribute to the variation in the AO.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>In over 400 German HD patients, polymorphisms in the nuclear respiratory factor 1 gene, <jats:italic>NRF-1<\/jats:italic>, and the mitochondrial transcription factor A, encoded by <jats:italic>TFAM<\/jats:italic> showed nominally significant association with AO of HD. When combining these results with the previously described modifiers rs7665116 in <jats:italic>PPARGC1A<\/jats:italic> and C7028T in the <jats:italic>cytochrome c oxidase subunit I<\/jats:italic> (<jats:italic>CO1<\/jats:italic>, mt haplogroup H) in a multivariable model, a substantial proportion of the variation in AO can be explained by the joint effect of significant modifiers and their interactions, respectively.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>These results underscore that impairment of mitochondrial function plays a critical role in the pathogenesis of HD and that upstream transcriptional activators of PGC-1<jats:italic>alpha<\/jats:italic> may be useful targets in the treatment of HD.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1750-1326-6-32","type":"journal-article","created":{"date-parts":[[2011,5,19]],"date-time":"2011-05-19T19:26:02Z","timestamp":1305833162000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":130,"title":["PGC-1alpha downstream transcription factors NRF-1 and TFAM are genetic modifiers of Huntington disease"],"prefix":"10.1186","volume":"6","author":[{"given":"Elahe","family":"Taherzadeh-Fard","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Saft","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denis A","family":"Akkad","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Wieczorek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aiden","family":"Haghikia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Chan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f6rg T","family":"Epplen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Larissa","family":"Arning","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2011,5,19]]},"reference":[{"key":"188_CR1","first-page":"971","volume":"26","author":"The Huntington's Disease Collaborative Research Group","year":"1993","unstructured":"The Huntington's Disease Collaborative Research Group: A novel gene containing a trinucleotide repeat that is unstable on Huntington's disease chromosomes. 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