Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice
By M. Gray, Dyna I. Shirasaki, C. Cepeda, V. André, B. Wilburn, Xiao-Hong Lu, Jifang Tao, I. Yamazaki, Shihua Li, Y. Sun and 3 more. Journal of Neuroscience, 2008
618 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d00556f4085aab6cba90fb846350a8a3681b03ea
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In Cellular and Molecular Neuroscience
- Mark P. Mattson
- C. Zuccato
- Fred H. Gage
- E. Cattaneo
- Wenzhen Duan
- M. Valenza
- Beate Winner
- D. Holtzman
In Molecular Biology
- Christopher A. Ross
- Fred H. Gage
- Mark P. Mattson
- M. Valenza
- E. Cattaneo
- D. Holtzman
- C. Zuccato
- D. Krainc
Citations in the corpus
- Neuroprotective role of SIRT1 in mammalian models of Huntington’s disease through activation of multiple SIRT1 targets (2011, positive): “…have motor deficits and Huntington’s disease–like brain pathology Neuroprotective role of Sirt1 in mammalian models of Huntington’s disease through activation of multiple Sirt1 targets l e t t e r s relatively earlier than mice from other available full-length Huntington’s disease models 12,13 .”
- Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis (2012, neutral): “Animals BACHD animals were acquired from William Yang (Gray et al., 2008).”
- Neurodegenerative disease and adult neurogenesis (2011, background): “…to the human disease have also been a full-length human mutant huntingtin mouse with 97 glutamine repeats on a bacterial artificial chromosome (Gray et al., 2008) and yeast artificial chromosome mice expressing normal yeast artificial chromosome (YAC) 18 and mutant (yeast artificial…”
- Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “By 12 mo of age, BACHD brains have only a few small aggregates predominantly in the neuropil in the cortex and very tiny aggregates in the striatum (221), suggesting that diffuse nuclear accumulation of aggregated mutant huntingtin in striata or cortices is not necessarily associated with the slowly”