ArticleExperimental neurology2017
2,4 DNP improves motor function, preserves medium spiny neuronal identity, and reduces oxidative stress in a mouse model of Huntington's disease.
Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Restoring mitochondrial health after blast-induced traumatic brain injury: modifiable factors and therapeutic opportunities.npj metabolic health and disease · 2026Review
- Zika virus impairs non-homologous end joining and exacerbates DNA damage in neural progenitors derived from Huntington's disease iPSCs via mutant huntingtin-elicited Ku70/Ku80 complex disruption.Stem cell research & therapy · 2025Article
- Micro-Doses of DNP Preserve Motor and Muscle Function with a Period of Functional Recovery in Amyotrophic Lateral Sclerosis Mice.Annals of neurology · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Article
- Application of a fully 3D printed carbon electrode for the double potential step Chronoamperometric determination of 2,4-dinitrophenol in environmental water samples.Frontiers in chemistry · 2025Article
- Leveraging explainable deep learning methodologies to elucidate the biological underpinnings of Huntington's disease using single-cell RNA sequencing data.BMC genomics · 2024Article
- OMA1 protease eliminates arrested protein import intermediates upon mitochondrial depolarization.The Journal of cell biology · 2024Article
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Mitochondrial Dysfunction After Repeated Mild Blast Traumatic Brain Injury Is Attenuated by a Mild Mitochondrial Uncoupling Prodrug.Journal of neurotrauma · 2023Article
- Mitochondrial proton leak in cardiac aging.GeroScience · 2023Review
- The relationship between experimental 2,4-Dinitrophenol administration and neurological oxidative stress: in terms of dose, time and gender differences.Molecular and cellular biochemistry · 2023Article
- Involvement of CRMP2 in Regulation of Mitochondrial Morphology and Motility in Huntington's Disease.Cells · 2021Article
- Mitochondria exert age-divergent effects on recovery from spinal cord injury.Experimental neurology · 2021Article
- Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing.Nature reviews. Drug discovery · 2020Review
- An evolutionary, or "Mitocentric" perspective on cellular function and disease.Redox biology · 2020Review
- Novel imaging biomarkers for mapping the impact of mild mitochondrial uncoupling in the outer retina in vivo.PloS one · 2020Article
- 2,4 Dinitrophenol as Medicine.Cells · 2019Review
- Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases.International journal of medical sciences · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the first exon of the gene huntingtin. There is no treatment to prevent or delay the disease course of HD currently. Oxidative stress and mitochondrial dysfunction have emerged as key determinants of the disease progression in HD. Therefore, counteracting mutant huntingtin (mHtt)-induced oxidative stress and mitochondrial dysfunction appears as a new approach to treat this devastating disease. Interestingly, mild mitochondrial uncoupling improves neuronal resistance to stress and facilitates neuronal survival. Mild mitochondrial uncoupling can be induced by the proper dose of 2,4-dinitrophenol (DNP), a proton ionophore that was previously used for weight loss. In this study, we evaluated the effects of chronic administration of DNP at three doses (0.5, 1, 5mg/kg/day) on mHtt-induced behavioral deficits and cellular abnormalities in the N171-82Q HD mouse model. DNP at a low dose (1mg/kg/day) significantly improved motor function and preserved medium spiny neuronal marker DARPP32 and postsynaptic protein PSD95 in the striatum of HD mice. Further mechanistic study suggests that DNP at this dose reduced oxidative stress in HD mice, which was indicated by reduced levels of F2-isoprostanes in the brain of HD mice treated with DNP. Our data indicated that DNP provided behavioral benefit and neuroprotective effect at a weight neutral dose in HD mice, suggesting that the potential value of repositioning DNP to HD treatment is warranted in well-controlled clinical trials in HD.
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