Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice
By R. Ferrante, James K. Kubilus, Junghee Lee, H. Ryu, A. Beesen, B. Zucker, Karen M. Smith, N. Kowall, R. Ratan, R. Luthi-Carter and 1 more. Journal of Neuroscience, 2003
706 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/8d9404fc6d5fcf088df301d84dcc9a14879a9020
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
In Molecular Biology
- J. Cryan
- Ted G. Dinan
- G. Clarke
- C. Stanton
- R. Stilling
- M. van de Wouw
- E. Cattaneo
- Leslie M. Thompson
In Neurology
Citations in the corpus
- Therapeutic application of histone deacetylase inhibitors for central nervous system disorders (2008, background): “The neuroprotective effects of the HDAC inhibition has been well documented in both invertebrate and mouse models of Huntington's disease and other polyglutamine-repeat disease”
- Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration. (2004, background): “Thus, VP16-CREB (Ferrante et al., 2003; Hockly et al., 2003; Kouraklis and Theocharis, 2002).”
- The neuropharmacology of butyrate: The bread and butter of the microbiota-gut-brain axis? (2016, background): “To this category also belong other neurodegenerative diseases, including Huntington’s disease (Ferrante et al., 2003; Gardian et al., 2005), Parkinson’s disease (Sharma et al.”
- Multiple roles of HDAC inhibition in neurodegenerative conditions (2009, positive): “Using the same model, Ferrante and colleagues reported that sodium butyrate treatment decreased the neurodegenerative phenotype and improved survival [59].”
- Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “These results indicate that reduced acetyltransferase activity might be an important component of polyglutamine pathogenesis and pave the way for HDAC inhibitors as part of important therapeutic strategies to pursue the restoration of gene transcription in HD (186, 260, 490, 550)(also see sect.”