Trial reportJournal of bioenergetics and biomembranes2013
A study of molecular changes relating to energy metabolism and cellular stress in people with Huntington's disease: looking for biomarkers.
Trial report in Journal of bioenergetics and biomembranes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- An integrative neuropharmacological review of Huntington's disease challenges and the role of novel formulations in addressing pharmacological‒pharmaceutical limitations.Frontiers in pharmacology · 2026Review
- Research advances in branched-chain amino acid metabolism in tumors.Molecular and cellular biochemistry · 2025Review
- The Role of Brain-Derived Neurotrophic Factor as an Essential Mediator in Neuronal Functions and the Therapeutic Potential of Its Mimetics for Neuroprotection in Neurologic and Psychiatric Disorders.Molecules (Basel, Switzerland) · 2025Review
- Exploring molecular mechanisms, therapeutic strategies, and clinical manifestations of Huntington's disease.Archives of pharmacal research · 2024Review
- A Novel Huntington's Disease Assessment Platform to Support Future Drug Discovery and Development.International journal of molecular sciences · 2022Article
- A Glimpse of Molecular Biomarkers in Huntington's Disease.International journal of molecular sciences · 2022Review
- The Role of Branched-Chain Amino Acids and Branched-Chain α-Keto Acid Dehydrogenase Kinase in Metabolic Disorders.Frontiers in nutrition · 2022Review
- Article
- New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021Review
- Small Non-coding RNAs Are Dysregulated in Huntington's Disease Transgenic Mice Independently of the Therapeutic Effects of an Environmental Intervention.Molecular neurobiology · 2021Article
- What, When and How to Measure-Peripheral Biomarkers in Therapy of Huntington's Disease.International journal of molecular sciences · 2021Review
- Integrative genomics analysis identifies five promising genes implicated in insomnia risk based on multiple omics datasets.Bioscience reports · 2020Article
- Longitudinal expression changes are weak correlates of disease progression in Huntington's disease.Brain communications · 2020Article
- Evaluation of Biochemical and Epigenetic Measures of Peripheral Brain-Derived Neurotrophic Factor (BDNF) as a Biomarker in Huntington's Disease Patients.Frontiers in molecular neuroscience · 2019Article
- Amitriptyline improves motor function via enhanced neurotrophin signaling and mitochondrial functions in the murine N171-82Q Huntington disease model.The Journal of biological chemistry · 2015Article
- Evaluating the SERCA2 and VEGF mRNAs as Potential Molecular Biomarkers of the Onset and Progression in Huntington's Disease.PloS one · 2015Article
- Enhanced neuronal glucose transporter expression reveals metabolic choice in a HD Drosophila model.PloS one · 2015Article
- Aberrant calcium signaling by transglutaminase-mediated posttranslational modification of inositol 1,4,5-trisphosphate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- A Tale of Two Maladies? Pathogenesis of Depression with and without the Huntington's Disease Gene Mutation.Frontiers in neurology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a neurodegenerative disorder characterized by a progressive motor and cognitive decline and the development of psychiatric symptoms. The origin of molecular and biochemical disturbances in HD is a mutation in the HTT gene, which is autosomally dominantly inherited. The altered huntingtin protein is ubiquitously expressed in the CNS, as well as in peripheral tissues. In this study we measured the metabolism changes in gene transcription in blood of HD gene carriers (premanifest and manifest combined) versus 28 healthy controls. The comparison revealed statistically significant Global Pattern Recognition Fold Change (FC) for 6 mRNA transcripts, reflecting an increase of: MAOB (FC = 3.07; p = 0.0005) which encodes an outer mitochondrial membrane-bound enzyme called monoamine oxidase type B; TGM2 (FC = 1.8; p = 0.02) encoding a transglutaminase 2 that mediates cellular stress; SLC2A4 (FC = 1.64; p = 0.02) solute carrier family 2 (facilitated glucose transporter) member 4; branched chain ketoacid dehydrogenase kinase (BCKDK) (FC = 1.34; p = 0.02); decrease of LDHA (FC = -1.16; p = 0.03) lactate dehydrogenase A; and brain-derived neurotrophic factor (BDNF) (FC = -2,11; p = 0.03). These distinguished changes coincided with HD progress. The analyses of gene transcription levels in sub-cohorts confirmed these changes and also revealed 28 statistically significant FCs of gene transcripts involved in ATP production and BCAA metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.