Neurological abnormalities in a knock-in mouse model of Huntington's disease.

By Chin-Shi Lin, S. Tallaksen-Greene, Wei-Ming Chien, J. A. Cearley, W. Jackson, Andrew B. Crouse, S. Ren, Xiao-Jiang Li, R. Albin, P. Detloff. Human Molecular Genetics, 2001

610 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/f3f0f1507acaf84bc027649ec7490635eeb099ba

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In Cellular and Molecular Neuroscience

1. C. Zuccato
2. E. Cattaneo
3. M. Valenza

In Molecular Biology

1. M. Valenza
2. E. Cattaneo
3. C. Zuccato

Citations in the corpus

• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, methodology): “The Hdh(CAG)150 mice produced by Peter Detloff’s laboratory at the University of Alabama at Birmingham exhibit mutant huntingtin aggregates at 9 mo of age (655) and weight loss, diminished activity, abnormal rotarod performance as well as a clasping phenotype that is indicative of neurological defic”
• Selective striatal neuronal loss in a YAC128 mouse model of Huntington disease. (2003, background): “A major question raised by this study is why is neuronal loss present in the YAC mice, but less evident in other models of HD? Neuronal loss is not specifically accounted for by the appropriate developmental and cell specific regulation of fulllength huntingtin in the YAC model, as the mice with tar”
• Tests to assess motor phenotype in mice: a user's guide (2009, background): “; assessment of specific abnormalities, such as body clasping in mice when suspended by the tai”
• Astrocytes: a central element in neurological diseases (2016, neutral): “mouse models expressing mutated huntingtin [75, 76, 137],”