Transcription meets metabolism in neurodegeneration
Article Abstract:
Two studies were conducted to determine whether abnormal mitochondrial function is important for the pathogenesis of Huntington disease or whether the mutant protein product of the Huntington disease gene, huntingtin, prompts transcriptional dysregulation. Results conclude that transcriptional dysregulation may cause mitochondrial dysfunction in Huntington disease because of reduced transcription of peroxisome proliferator-activated receptor co-activator-1[alpha] {PGC-1[alpha]} and of downstream genes coregulated by PGC-1[alpha].
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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Protein aggregation and neurodegenerative disease
Article Abstract:
Mechanisms of protein misfolding and aggregation in relation to neurodegenerative disease pathogenesis along with therapeutic implications are reviewed. The increased understanding of the pathways involved in protein aggregation have led to emerging clues of molecular mechanisms of cellular toxicity.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2004
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Increased apoptosis of Huntington disease lymphoblasts associated with repeat length-dependent mitochondrial depolarization
Article Abstract:
Lymphoblasts from patients with Huntington disease exhibit increased mitochondrial depolarization and cell death when subjected to stress. This illustrates that the gene defect that causes the disease affects other organs besides the brain.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 1999
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