The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Triterpenoids CDDO-ethyl amide and CDDO-trifluoroethyl amide improve the behavioral phenotype and brain pathology in a transgenic mouse model of Huntington's disease
Open accessAbstract
Oxidative stress is a prominent feature of Huntington's disease (HD) due to mitochondrial dysfunction and the ensuing overproduction of reactive oxygen species (ROS). This phenomenon ultimately contributes to cognitive and motor impairment, as well as brain pathology, especially in the striatum. Targeting the transcription of the endogenous antioxidant machinery could be a promising therapeutic approach. The NF-E2-related factor-2 (Nrf2)/antioxidant response element (ARE) signaling pathway is an important pathway involved in antioxidant and anti-inflammatory responses. Synthetic triterpenoids, which are derived from 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic acid (CDDO) activate the Nrf2/ARE pathway and reduce oxidative stress in animal models of neurodegenerative diseases. We investigated the effects of CDDO-ethyl amide (CDDO-EA) and CDDO-trifluoroethyl amide (CDDO-TFEA) in N171-82Q mice, a transgenic mouse model of HD. CDDO-EA or CDDO-TFEA were administered in the diet at various concentrations, starting at 30 days of age. CDDO-EA and CDDO-TFEA upregulated Nrf2/ARE induced genes in the brain and peripheral tissues, reduced oxidative stress, improved motor impairment and increased longevity. They also rescued striatal atrophy in the brain and vacuolation in the brown adipose tissue. Therefore compounds targeting the Nrf2/ARE pathway show great promise for the treatment of HD.
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Cites
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“N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript We also found that in skeletal muscle, after CDDO-TFEA administration, the mRNA levels of the following genes were significantly increased as compared to control diet: GST3a (Figure 6C; Fisher's PLSD, p=0.007 at 100mg/kg diet, p=0.0001…”
BackgroundInfluentialSelf-citationMicroglial activation correlates with severity in Huntington disease: A clinical and PET study
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BackgroundMicroglial activation in presymptomatic Huntington's disease gene carriers
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Self-citationTherapeutic Effects of Coenzyme Q10and Remacemide in Transgenic Mouse Models of Huntington's Disease
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Cited by
The KEAP1-NRF2 system: a thiol-based sensor-effector apparatus for maintaining redox homeostasis
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NRF2 and cancer: the good, the bad and the importance of context
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Self-citationBuendia, I., Michalska, P., Navarro, E., Gameiro, I., Egea, J., & León, R. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.11.003 · Cited by 678
Sivandzade, F., Prasad, S., Bhalerao, A., & Cucullo, L. (2019) · Redox Biology · doi:10.1016/j.redox.2018.11.017 · Cited by 639
Neuroprotective strategies involving ROS in Alzheimer disease
Dumont, M., & Beal, M. F. (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2010.11.026 · Cited by 402
Self-citation
Metadata
- Authors
- Stack, C., Ho, D., Wille, E., Calingasan, N. Y., Williams, C., Liby, K., Sporn, M., Dumont, M., & Beal, M. F.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2010-07
- Volume
- 49
- Issue
- 2
- Pages
- 147-158
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W1972272898
- Cited by
- 169
- References
- 12
- FWCI
- 5.62
- Type
- journal article
- Language
- en
- Open access
- green
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- Stack, C., Ho, D., Wille, E., Calingasan, N. Y., Williams, C., Liby, K., Sporn, M., Dumont, M., & Beal, M. F. (2010). Triterpenoids CDDO-ethyl amide and CDDO-trifluoroethyl amide improve the behavioral phenotype and brain pathology in a transgenic mouse model of Huntington's disease. Free Radical Biology and Medicine. https://doi.org/10.1016/j.freeradbiomed.2010.03.017
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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