Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease

By E. Hockly, V. Richon, B. Woodman, Donna L. Smith, Xianbo Zhou, E. Rosa, K. Sathasivam, S. Ghazi‐Noori, A. Mahal, PhilipA.S Lowden and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2003

860 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/460ff04f61b3ff3992e745a09dd774a764a39880

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Citations in the corpus

Phase I clinical trial of histone deacetylase inhibitor: suberoylanilide hydroxamic acid administered intravenously. (2003, background): “of acetylated histones in the brain (17), suggesting diffusion”
Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease (2004, background): “Other researchers also do not use lifespan as an indicator in therapeutic trials in mice, which they euthanize at humane end point”
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”
Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation (2007, background): “This is a timely question considering the clinical use of HDAC inhibitors for cancer therapy (for review, see Lund and van Lohuizen, 2004) and their potential use for treatment of mental retardation and neurodegenerative diseases (Steffan et al., 2001; Hockly et al., 2003).”
Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice (2003, positive): “Although sodium butyrate treatment was neuroprotective, it did not prevent body weight loss, a finding similar to other transcriptionally active compounds (Ferrante et al., 2002b; Hockly et al., 2003).”
Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration. (2004, methodology): “…the top four acetand Theocharis, 2002) and neurodegenerative diseasesylated histone species in which the steady state of ace(Ferrante et al., 2003; Hockly et al., 2003) may enhancetylation was more significantly altered in response to L-LTP significantly both in cbp-deficient mutants…”
Multiple roles of HDAC inhibition in neurodegenerative conditions (2009, background): “Using R6/2 mice, Hockly and colleagues showed that vorinostat improved motor performance in a rotarod test but did not affect polyQ aggregation or downregulate the expanded HTT transgene expressed in the R6/2 mice [58].”
Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, methodology): “This study demonstrated that SAHA crosses the blood-brain barrier, increases histone acetylation in the brain, and reduces the motor impairment in R6/2 mice (260).”
Trehalose alleviates polyglutamine-mediated pathology in a mouse model of Huntington disease (2004, neutral): “A histone deacetylase inhibitor improves motor impairmen”
Anti-inflammatory Agents: Present and Future (2010, positive): “, 1999) and treatment with oral SAHA reduces disease severity (Hockly et al., 2003) (Table S2).”