ArticleProceedings of the National Academy of Sciences of the United States of America2007
Inhibitors of metabolism rescue cell death in Huntington's disease models.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. 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, 61 citations in OpenAlex.
- Fisetin: hormesis accounts for many of its chemoprotective effects.Biogerontology · 2025Review
- A Novel Huntington's Disease Assessment Platform to Support Future Drug Discovery and Development.International journal of molecular sciences · 2022Article
- UsingFrontiers in pharmacology · 2022Review
- Genetic Screen in Adult Drosophila Reveals That dCBP Depletion in Glial Cells Mitigates Huntington Disease Pathology through a Foxo-Dependent Pathway.International journal of molecular sciences · 2021Article
- Twist1 Plays an Anti-apoptotic Role in Mutant Huntingtin Expression Striatal Progenitor Cells.Molecular neurobiology · 2020Article
- Article
- Purinergic Receptors in Neurological Diseases With Motor Symptoms: Targets for Therapy.Frontiers in pharmacology · 2018Review
- Necroptosis in neurodegenerative diseases: a potential therapeutic target.Cell death & disease · 2017Review
- The extracellular signal-regulated kinase 1/2 pathway in neurological diseases: A potential therapeutic target (Review).International journal of molecular medicine · 2017Review
- Connectivity mapping uncovers small molecules that modulate neurodegeneration in Huntington's disease models.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases.Chemistry Central journal · 2015Review
- Enhanced neuronal glucose transporter expression reveals metabolic choice in a HD Drosophila model.PloS one · 2015Article
- Socially responsive effects of brain oxidative metabolism on aggression.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Role of P2X7 purinoceptors in neuroprotective mechanism of ischemic postconditioning in mice.Molecular and cellular biochemistry · 2014Article
- MAP kinase phosphatase 1 (MKP-1/DUSP1) is neuroprotective in Huntington's disease via additive effects of JNK and p38 inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A novel target for Huntington's disease: ERK at the crossroads of signaling. The ERK signaling pathway is implicated in Huntington's disease and its upregulation ameliorates pathology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2012Article
- Pizotifen Activates ERK and Provides Neuroprotection in vitro and in vivo in Models of Huntington's Disease.Journal of Huntington's disease · 2012Article
- Probing mechanisms that underlie human neurodegenerative diseases in Drosophila.Annual review of genetics · 2012Review
- Meclizine is neuroprotective in models of Huntington's disease.Human molecular genetics · 2011Article
- ERK activation by the polyphenols fisetin and resveratrol provides neuroprotection in multiple models of Huntington's disease.Human molecular genetics · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a fatal inherited neurodegenerative disorder. HD is caused by polyglutamine expansions in the huntingtin (htt) protein that result in neuronal loss and contribute to HD pathology. The mechanisms of neuronal loss in HD are elusive, and there is no therapy to alleviate HD. To find small molecules that slow neuronal loss in HD, we screened 1,040 biologically active molecules to identify suppressors of cell death in a neuronal cell culture model of HD. We found that inhibitors of mitochondrial function or glycolysis rescued cell death in this cell culture and in in vivo HD models. These inhibitors prevented cell death by activating prosurvival ERK and AKT signaling but without altering cellular ATP levels. ERK and AKT inhibition through the use of specific chemical inhibitors abrogated the rescue, whereas their activation through the use of growth factors rescued cell death, suggesting that this activation could explain the protective effect of metabolic inhibitors. Both ERK and AKT signaling are disrupted in HD, and activating these pathways is protective in several HD models. Our results reveal a mechanism for activating prosurvival signaling that could be exploited for treating HD and possibly other neurodegenerative disorders.
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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.