ArticleScientific reports2017
The stress response factor daf-16/FOXO is required for multiple compound families to prolong the function of neurons with Huntington's disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Chromatin and epigenetics in aging biology.Genetics · 2025Review
- Unraveling Molecular Targets for Neurodegenerative Diseases ThroughInternational journal of molecular sciences · 2025Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Bisphosphonates attenuate age-related muscle decline in Caenorhabditis elegans.Journal of cachexia, sarcopenia and muscle · 2023Article
- Dopaminergic modulation by quercetin: In silico and in vivo evidence using Caenorhabditis elegans as a model.Chemico-biological interactions · 2023Article
- Changes in lipid metabolism driven by steroid signalling modulate proteostasis in C. elegans.EMBO reports · 2023Article
- Dietary Flavonoids and Adult Neurogenesis: Potential Implications for Brain Aging.Current neuropharmacology · 2023Review
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Flavonoids modulate AMPK/PGC-1α and interconnected pathways toward potential neuroprotective activities.Metabolic brain disease · 2021Review
- Neuroprotective Properties of Kempferol Derivatives fromInternational journal of molecular sciences · 2021Article
- Natural Products in the Prevention of Metabolic Diseases: Lessons Learned from the 20th KAST Frontier Scientists Workshop.Nutrients · 2021Review
- Drug discovery: Insights from the invertebrate Caenorhabditis elegans.Pharmacology research & perspectives · 2021Review
- The quest to slow ageing through drug discovery.Nature reviews. Drug discovery · 2020Review
- Research Progress on Alzheimer's Disease and Resveratrol.Neurochemical research · 2020Review
- Biological Aging and the Cellular Pathogenesis of Huntington's Disease.Journal of Huntington's disease · 2020Review
- Impaired Redox Signaling in Huntington's Disease: Therapeutic Implications.Frontiers in molecular neuroscience · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helping neurons to compensate for proteotoxic stress and maintain function over time (neuronal compensation) has therapeutic potential in aging and neurodegenerative disease. The stress response factor FOXO3 is neuroprotective in models of Huntington's disease (HD), Parkinson's disease and motor-neuron diseases. Neuroprotective compounds acting in a FOXO-dependent manner could thus constitute bona fide drugs for promoting neuronal compensation. However, whether FOXO-dependent neuroprotection is a common feature of several compound families remains unknown. Using drug screening in C. elegans nematodes with neuronal expression of human exon-1 huntingtin (128Q), we found that 3ß-Methoxy-Pregnenolone (MAP4343), 17ß-oestradiol (17ßE2) and 12 flavonoids including isoquercitrin promote neuronal function in 128Q nematodes. MAP4343, 17ßE2 and isoquercitrin also promote stress resistance in mutant Htt striatal cells derived from knock-in HD mice. Interestingly, daf-16/FOXO is required for MAP4343, 17ßE2 and isoquercitrin to sustain neuronal function in 128Q nematodes. This similarly applies to the GSK3 inhibitor lithium chloride (LiCl) and, as previously described, to resveratrol and the AMPK activator metformin. Daf-16/FOXO and the targets engaged by these compounds define a sub-network enriched for stress-response and neuronally-active pathways. Collectively, these data highlights the dependence on a daf-16/FOXO-interaction network as a common feature of several compound families for prolonging neuronal function in HD.
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