The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
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The importance of integrating basic and clinical research toward the development of new therapies for Huntington diseaseThe many faces of autophagy dysfunction in Huntington's disease: from mechanism to therapyNew insights into PGC-1 coactivators: redefining their role in the regulation of mitochondrial function and beyondPGC-1α, mitochondrial dysfunction, and Huntington's diseaseAutophagy in polyglutamine disease: Imposing order on disorder or contributing to the chaos?NMDA receptor gene variations as modifiers in Huntington disease: a replication studyShaping the role of mitochondria in the pathogenesis of Huntington's diseaseMitochondrial dysfunction in neurodegenerative diseasesSumoylation regulates nuclear localization of lipin-1alpha in neuronal cells.Population stratification may bias analysis of PGC-1α as a modifier of age at Huntington disease motor onset.Modeling Huntington disease in yeast: perspectives and future directions.Association of PGC-1alpha polymorphisms with age of onset and risk of Parkinson's diseaseImpairment of PGC-1alpha expression, neuropathology and hepatic steatosis in a transgenic mouse model of Huntington's disease following chronic energy deprivation.A greatly extended PPARGC1A genomic locus encodes several new brain-specific isoforms and influences Huntington disease age of onset.Genetic analysis of polymorphisms in the kalirin gene for association with age-at-onset in European Huntington disease patients.Huntington's disease and its therapeutic target genes: a global functional profile based on the HD Research Crossroads databasePGC-1α provides a transcriptional framework for synchronous neurotransmitter release from parvalbumin-positive interneurons.Developmental alterations in motor coordination and medium spiny neuron markers in mice lacking pgc-1αPgc-1α overexpression downregulates Pitx3 and increases susceptibility to MPTP toxicity associated with decreased Bdnf.Localization of sequence variations in PGC-1α influence their modifying effect in Huntington disease.The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients.Mutual exacerbation of peroxisome proliferator-activated receptor γ coactivator 1α deregulation and α-synuclein oligomerizationPGC-1alpha downstream transcription factors NRF-1 and TFAM are genetic modifiers of Huntington disease.A single nucleotide polymorphism in the coding region of PGC-1α is a male-specific modifier of Huntington disease age-at-onset in a large European cohort.Characterization of novel peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) isoform in human liver.Exploring Genetic Factors Involved in Huntington Disease Age of Onset: E2F2 as a New Potential Modifier Gene.Pharmacologic activation of mitochondrial biogenesis exerts widespread beneficial effects in a transgenic mouse model of Huntington's diseaseSustained expression of PGC-1α in the rat nigrostriatal system selectively impairs dopaminergic function.Mitochondrial biogenesis: a therapeutic target for neurodevelopmental disorders and neurodegenerative diseasesReduced activity of AMP-activated protein kinase protects against genetic models of motor neuron disease.Enhanced mitochondrial biogenesis ameliorates disease phenotype in a full-length mouse model of Huntington's disease.Synaptic activity and bioenergy homeostasis: implications in brain trauma and neurodegenerative diseases.Foxa1 is essential for development and functional integrity of the subthalamic nucleus.β-Defensin Genomic Copy Number Does Not Influence the Age of Onset in Huntington's Disease.Insulin and Insulin-Sensitizing Drugs in Neurodegeneration: Mitochondria as Therapeutic Targets.Attenuation of polyglutamine-induced toxicity by enhancement of mitochondrial OXPHOS in yeast and fly models of aging.Molecular mechanisms and potential therapeutical targets in Huntington's disease.PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington's disease to Parkinson's disease and beyond.Targeting Huntington's disease through histone deacetylases.Prospects for neuroprotective therapies in prodromal Huntington's disease.
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The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 08 January 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
@en
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease.
@nl
type
label
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
@en
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease.
@nl
prefLabel
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
@en
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease.
@nl
P2093
P2860
P356
P1476
The gene coding for PGC-1alpha modifies age at onset in Huntington's Disease
@en
P2093
Claus Weidinger
G Bernhard Landwehrmeyer
Hannes Oberkofler
Patrick Weydt
Selma M Soyal
Stefano Didonato
Wolfgang Patsch
P2860
P2888
P356
10.1186/1750-1326-4-3
P577
2009-01-08T00:00:00Z
P5875
P6179
1052726702