ArticleHuman molecular genetics2015
Oxidative metabolism in YAC128 mouse model of Huntington's disease.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Treatment of Huntington's disease with a pan-HTT-targeting CRISPR nuclease.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- HDDF2-A Novel Patient-Derived Fibroblast Line from Huntington's Disease with Prominent Cellular Senescence and polyQ Pathology.Biomedicines · 2026Article
- Article
- Temporal Characterization of Behavioral and Hippocampal Dysfunction in the YAC128 Mouse Model of Huntington's Disease.Biomedicines · 2022Article
- A New Perspective on Huntington's Disease: How a Neurological Disorder Influences the Peripheral Tissues.International journal of molecular sciences · 2022Review
- Involvement of CRMP2 in Regulation of Mitochondrial Morphology and Motility in Huntington's Disease.Cells · 2021Article
- Article
- Age-related mitochondrial alterations in brain and skeletal muscle of the YAC128 model of Huntington disease.NPJ aging and mechanisms of disease · 2021Article
- Mitochondrial membranes modify mutant huntingtin aggregation.Biochimica et biophysica acta. Biomembranes · 2021Article
- Glucose metabolic crosstalk and regulation in brain function and diseases.Progress in neurobiology · 2021Review
- The Sigma-1 Receptor Mediates Pridopidine Rescue of Mitochondrial Function in Huntington Disease Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Mutant huntingtin does not cross the mitochondrial outer membrane.Human molecular genetics · 2020Article
- Manganese-induced Mitochondrial Dysfunction Is Not Detectable at Exposures Below the Acute Cytotoxic Threshold in Neuronal Cell Types.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Bioenergetic deficits in Huntington's disease iPSC-derived neural cells and rescue with glycolytic metabolites.Human molecular genetics · 2020Article
- Expression of mutant exon 1 huntingtin fragments in human neural stem cells and neurons causes inclusion formation and mitochondrial dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Energy Metabolism and Mitochondrial Superoxide Anion Production in Pre-symptomatic Striatal Neurons Derived from Human-Induced Pluripotent Stem Cells Expressing Mutant Huntingtin.Molecular neurobiology · 2020Article
- Mutant huntingtin fails to directly impair brain mitochondria.Journal of neurochemistry · 2019Article
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Novel proteomic changes in brain mitochondria provide insights into mitochondrial dysfunction in mouse models of Huntington's disease.Mitochondrion · 2019Article
- Metabolic Reprogramming in Astrocytes Distinguishes Region-Specific Neuronal Susceptibility in Huntington Mice.Cell metabolism · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Alterations in oxidative metabolism are considered to be one of the major contributors to Huntington's disease (HD) pathogenesis. However, existing data about oxidative metabolism in HD are contradictory. Here, we investigated the effect of mutant huntingtin (mHtt) on oxidative metabolism in YAC128 mice. Both mHtt and wild-type huntingtin (Htt) were associated with mitochondria and the amount of bound Htt was four-times higher than the amount of bound mHtt. Percoll gradient-purified brain synaptic and non-synaptic mitochondria as well as unpurified brain, liver and heart mitochondria, isolated from 2- and 10-month-old YAC128 mice and age-matched WT littermates had similar respiratory rates. There was no difference in mitochondrial membrane potential or ADP and ATP levels. Expression of selected nuclear-encoded mitochondrial proteins in 2- and 10-month-old YAC128 and WT mice was similar. Cultured striatal and cortical neurons from YAC128 and WT mice had similar respiratory and glycolytic activities as measured with Seahorse XF24 analyzer in medium containing 10 mm glucose and 15 mm pyruvate. In the medium with 2.5 mm glucose, YAC128 striatal neurons had similar respiration, but slightly lower glycolytic activity. Striatal neurons had lower maximal respiration compared with cortical neurons. In vivo experiments with YAC128 and WT mice showed similar O2 consumption, CO2 release, physical activity, food consumption and fasted blood glucose. However, YAC128 mice were heavier and had more body fat compared with WT mice. Overall, our data argue against respiratory deficiency in YAC128 mice and, consequently, suggest that mitochondrial respiratory dysfunction is not essential for HD pathogenesis.
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