The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington’s disease
Open accessAbstract
Huntington's disease (HD) is associated with transcriptional dysregulation, and multiple studies with histone deacetylase (HDAC) inhibitors suggest that global approaches for restoring transcriptional balance and appropriate protein acetylation are therapeutically promising. To determine whether more targeted approaches might be effective, we have tested the impact of all the HDACs in Drosophila on Huntingtin (Htt)-induced pathology. Among the zinc-dependent or 'classic' HDACs, we find that neurodegeneration is most sensitive to levels of Rpd3. We also find that among the NAD(+)-dependent class III deacetylases, genetic or pharmacological reduction of either Sir2 or Sirt2 provides neuroprotection to Htt-challenged animals and that even greater neuroprotection is achieved when Rpd3 and Sir2 are simultaneously reduced. Our experiments suggest that longevity promoting strategies may be distinct from those that protect against neurodegeneration in Drosophila challenged with mutant human Htt. These results highlight a novel therapeutic approach for HD in the form of Sir2 inhibition and possible combinatorial inhibition of Sir2 and Rpd3.
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Cites
Chromatin modifications and their function
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Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan
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Nutrient control of glucose homeostasis through a complex of PGC-1α and SIRT1
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Sirtuin activators mimic caloric restriction and delay ageing in metazoans
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Acetylation and deacetylation of non-histone proteins
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HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS.
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Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila
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Self-citationSIRT1 Functionally Interacts with the Metabolic Regulator and Transcriptional Coactivator PGC-1α
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Cited by
Slowing ageing by design: the rise of NAD+ and sirtuin-activating compounds
Bonkowski, M. S., & Sinclair, D. A. (2016) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2016.93 · Cited by 834
NAD+ in Brain Aging and Neurodegenerative Disorders
Lautrup, S., Sinclair, D. A., Mattson, M. P., & Fang, E. F. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.09.001 · Cited by 790
Multiple roles of HDAC inhibition in neurodegenerative conditions
Chuang, D.-M., Leng, Y., Marinova, Z., Kim, H.-J., & Chiu, C.-T. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2009.06.002 · Cited by 676
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“…complements a number of emerging studies showing that Sir2 inhibitors improve pathology in other neurodegenerative diseases including Huntington’s disease and other models of polyglutamine repeat disorders (Ghosh and Feany, 2004; Pallos et al., 2008) and Parkinson’s disease (Outeiro et al., 2007).”
BackgroundSelf-citationSeven sirtuins for seven deadly diseases ofaging
Morris, B. J. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2012.10.525 · Cited by 377
Metadata
- Authors
- Pallos, J., Bodai, L., Lukacsovich, T., Purcell, J. M., Steffan, J. S., Thompson, L. M., & Marsh, J. L.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-09-01
- Volume
- 17
- Issue
- 23
- Pages
- 3767-3775
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2106012958
- Cited by
- 265
- References
- 18
- FWCI
- 9.32
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington’s disease. https://app.cochat.ai/papers/10.1093/hmg/ddn273
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- Pallos, J., Bodai, L., Lukacsovich, T., Purcell, J. M., Steffan, J. S., Thompson, L. M., & Marsh, J. L. (2008). Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington’s disease. Human Molecular Genetics. https://doi.org/10.1093/hmg/ddn273
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
