ArticleThe Journal of experimental medicine2016
Potential biomarkers to follow the progression and treatment response of Huntington's disease.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Cationic Arginine-Rich Peptides (CARPs): A Novel Class of Neuroprotective Agents With a Multimodal Mechanism of Action.Frontiers in neurology · 2020Pooled it
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- 3-Nitropropionic Acid-Induced Huntington's Disease in Preclinical Models: Mechanisms, Peripheral Toxicities, Model Gaps, and Future Directions.Molecular neurobiology · 2026Review
- Profiles of patients at early stages of Huntington's disease based on the routine biological markers and the disease progression.Journal of neurology · 2026Article
- The Impact of Neurotoxin Proteins Trafficked by Primary Cilia and Extracellular Vesicles in Neurodegenerative Diseases.Biology · 2025Review
- Excessive mitochondrial fission and associated extracellular mitochondria mediate cardiac dysfunction in obesity cardiomyopathy.Life sciences · 2025Article
- Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.Journal of neuroinflammation · 2025Review
- Oxidative Stress-mediated Lipid Peroxidation-derived Lipid Aldehydes in the Pathophysiology of Neurodegenerative Diseases.Current neuropharmacology · 2025Review
- Lowering mutant huntingtin by small molecules relieves Huntington's disease symptoms and progression.EMBO molecular medicine · 2024Article
- Targeting an allosteric site in dynamin-related protein 1 to inhibit Fis1-mediated mitochondrial dysfunction.Nature communications · 2023Article
- Biomarkers: Role and Scope in Neurological Disorders.Neurochemical research · 2023Review
- mtDNA Maintenance and Alterations in the Pathogenesis of Neurodegenerative Diseases.Current neuropharmacology · 2023Review
- Current Diagnostic Methods and Non-Coding RNAs as Possible Biomarkers in Huntington's Disease.Genes · 2022Review
- Experimental and Clinical Biomarkers for Progressive Evaluation of Neuropathology and Therapeutic Interventions for Acute and Chronic Neurological Disorders.International journal of molecular sciences · 2022Review
- Mitochondrial HSF1 triggers mitochondrial dysfunction and neurodegeneration in Huntington's disease.EMBO molecular medicine · 2022Article
- Mitochondrial Fusion, Fission, and Mitophagy in Cardiac Diseases: Challenges and Therapeutic Opportunities.Antioxidants & redox signaling · 2022Review
- Neuroinflammation in Huntington's disease: From animal models to clinical therapeutics.Frontiers in immunology · 2022Review
- Age-related mitochondrial alterations in brain and skeletal muscle of the YAC128 model of Huntington disease.NPJ aging and mechanisms of disease · 2021Article
- Neuroimaging, Urinary, and Plasma Biomarkers of Treatment Response in Huntington's Disease: Preclinical Evidence with the p75Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- What, When and How to Measure-Peripheral Biomarkers in Therapy of Huntington's Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is a rare genetic disease caused by expanded polyglutamine repeats in the huntingtin protein resulting in selective neuronal loss. Although genetic testing readily identifies those who will be affected, current pharmacological treatments do not prevent or slow down disease progression. A major challenge is the slow clinical progression and the inability to biopsy the affected tissue, the brain, making it difficult to design short and effective proof of concept clinical trials to assess treatment benefit. In this study, we focus on identifying peripheral biomarkers that correlate with the progression of the disease and treatment benefit. We recently developed an inhibitor of pathological mitochondrial fragmentation, P110, to inhibit neurotoxicity in HD. Changes in levels of mitochondrial DNA (mtDNA) and inflammation markers in plasma, a product of DNA oxidation in urine, mutant huntingtin aggregates, and 4-hydroxynonenal adducts in muscle and skin tissues were all noted in HD R6/2 mice relative to wild-type mice. Importantly, P110 treatment effectively reduced the levels of these biomarkers. Finally, abnormal levels of mtDNA were also found in plasma of HD patients relative to control subjects. Therefore, we identified several potential peripheral biomarkers as candidates to assess HD progression and the benefit of intervention for future clinical trials.
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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.