PGC-1alphaas modifier of onset age in Huntington disease

Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic fact...
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Autor*in:	Taherzadeh-Fard, Elahe [verfasserIn] Saft, Carsten Andrich, Jürgen Wieczorek, Stefan Arning, Larissa

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Schlagwörter:	Genetic Modifier Huntington Disease Huntington Disease Patient Transcriptional Deregulation Huntington Disease Gene

Anmerkung:	© Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: Molecular neurodegeneration - London : Biomed Central, 2006, 4(2009), 1 vom: 06. Feb.
Übergeordnetes Werk:	volume:4 ; year:2009 ; number:1 ; day:06 ; month:02

Links:	Volltext

DOI / URN:	10.1186/1750-1326-4-10

Katalog-ID:	SPR029506638

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allfields	10.1186/1750-1326-4-10 doi (DE-627)SPR029506638 (SPR)1750-1326-4-10-e DE-627 ger DE-627 rakwb eng Taherzadeh-Fard, Elahe verfasserin aut PGC-1alphaas modifier of onset age in Huntington disease 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213 Saft, Carsten aut Andrich, Jürgen aut Wieczorek, Stefan aut Arning, Larissa aut Enthalten in Molecular neurodegeneration London : Biomed Central, 2006 4(2009), 1 vom: 06. Feb. (DE-627)515978361 (DE-600)2244557-2 1750-1326 nnns volume:4 year:2009 number:1 day:06 month:02 https://dx.doi.org/10.1186/1750-1326-4-10 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 1 06 02
spelling	10.1186/1750-1326-4-10 doi (DE-627)SPR029506638 (SPR)1750-1326-4-10-e DE-627 ger DE-627 rakwb eng Taherzadeh-Fard, Elahe verfasserin aut PGC-1alphaas modifier of onset age in Huntington disease 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213 Saft, Carsten aut Andrich, Jürgen aut Wieczorek, Stefan aut Arning, Larissa aut Enthalten in Molecular neurodegeneration London : Biomed Central, 2006 4(2009), 1 vom: 06. Feb. (DE-627)515978361 (DE-600)2244557-2 1750-1326 nnns volume:4 year:2009 number:1 day:06 month:02 https://dx.doi.org/10.1186/1750-1326-4-10 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 1 06 02
allfields_unstemmed	10.1186/1750-1326-4-10 doi (DE-627)SPR029506638 (SPR)1750-1326-4-10-e DE-627 ger DE-627 rakwb eng Taherzadeh-Fard, Elahe verfasserin aut PGC-1alphaas modifier of onset age in Huntington disease 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213 Saft, Carsten aut Andrich, Jürgen aut Wieczorek, Stefan aut Arning, Larissa aut Enthalten in Molecular neurodegeneration London : Biomed Central, 2006 4(2009), 1 vom: 06. Feb. (DE-627)515978361 (DE-600)2244557-2 1750-1326 nnns volume:4 year:2009 number:1 day:06 month:02 https://dx.doi.org/10.1186/1750-1326-4-10 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 1 06 02
allfieldsGer	10.1186/1750-1326-4-10 doi (DE-627)SPR029506638 (SPR)1750-1326-4-10-e DE-627 ger DE-627 rakwb eng Taherzadeh-Fard, Elahe verfasserin aut PGC-1alphaas modifier of onset age in Huntington disease 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213 Saft, Carsten aut Andrich, Jürgen aut Wieczorek, Stefan aut Arning, Larissa aut Enthalten in Molecular neurodegeneration London : Biomed Central, 2006 4(2009), 1 vom: 06. Feb. (DE-627)515978361 (DE-600)2244557-2 1750-1326 nnns volume:4 year:2009 number:1 day:06 month:02 https://dx.doi.org/10.1186/1750-1326-4-10 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 1 06 02
allfieldsSound	10.1186/1750-1326-4-10 doi (DE-627)SPR029506638 (SPR)1750-1326-4-10-e DE-627 ger DE-627 rakwb eng Taherzadeh-Fard, Elahe verfasserin aut PGC-1alphaas modifier of onset age in Huntington disease 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213 Saft, Carsten aut Andrich, Jürgen aut Wieczorek, Stefan aut Arning, Larissa aut Enthalten in Molecular neurodegeneration London : Biomed Central, 2006 4(2009), 1 vom: 06. Feb. (DE-627)515978361 (DE-600)2244557-2 1750-1326 nnns volume:4 year:2009 number:1 day:06 month:02 https://dx.doi.org/10.1186/1750-1326-4-10 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 1 06 02
language	English
source	Enthalten in Molecular neurodegeneration 4(2009), 1 vom: 06. Feb. volume:4 year:2009 number:1 day:06 month:02
sourceStr	Enthalten in Molecular neurodegeneration 4(2009), 1 vom: 06. Feb. volume:4 year:2009 number:1 day:06 month:02
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Genetic Modifier Huntington Disease Huntington Disease Patient Transcriptional Deregulation Huntington Disease Gene
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container_title	Molecular neurodegeneration
authorswithroles_txt_mv	Taherzadeh-Fard, Elahe @@aut@@ Saft, Carsten @@aut@@ Andrich, Jürgen @@aut@@ Wieczorek, Stefan @@aut@@ Arning, Larissa @@aut@@
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author	Taherzadeh-Fard, Elahe
spellingShingle	Taherzadeh-Fard, Elahe misc Genetic Modifier misc Huntington Disease misc Huntington Disease Patient misc Transcriptional Deregulation misc Huntington Disease Gene PGC-1alphaas modifier of onset age in Huntington disease
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topic_title	PGC-1alphaas modifier of onset age in Huntington disease Genetic Modifier (dpeaa)DE-He213 Huntington Disease (dpeaa)DE-He213 Huntington Disease Patient (dpeaa)DE-He213 Transcriptional Deregulation (dpeaa)DE-He213 Huntington Disease Gene (dpeaa)DE-He213
topic	misc Genetic Modifier misc Huntington Disease misc Huntington Disease Patient misc Transcriptional Deregulation misc Huntington Disease Gene
topic_unstemmed	misc Genetic Modifier misc Huntington Disease misc Huntington Disease Patient misc Transcriptional Deregulation misc Huntington Disease Gene
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title	PGC-1alphaas modifier of onset age in Huntington disease
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title_full	PGC-1alphaas modifier of onset age in Huntington disease
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title_sort	pgc-1alphaas modifier of onset age in huntington disease
title_auth	PGC-1alphaas modifier of onset age in Huntington disease
abstract	Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Abstract Although there is a strong correlation between CAG repeat length and age at onset (AO) of motor symptoms, individual Huntington disease (HD) patients may differ dramatically in onset age and disease manifestations despite similar CAG repeat lengths. This has led to a search for genetic factors that influence AO. In order to identify such a genetic modifier, we analysed polymorphisms in the PGC-1alpha gene. Recent data indicate inhibition of PGC-1alpha function by mutant Htt supporting a link between transcriptional deregulation and mitochondrial dysfunction in HD. In > 400 HD patients, a polymorphism located within intron 2, a potential recombination hot spot, explains a small, but statistically significant, amount of the variability in AO. Our data suggest that PGC-1alpha has modifying effects on the pathogenic process in HD. © Taherzadeh-Fard et al; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	PGC-1alphaas modifier of onset age in Huntington disease
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PGC-1alphaas modifier of onset age in Huntington disease

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