Normal huntingtin function: an alternative approach to Huntington's disease
By E. Cattaneo, C. Zuccato, Marzia Tartari. Nature Reviews Neuroscience, 2005
688 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/780816bcbfdebda98d25d916ca334eadee607d35
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In Cellular and Molecular Neuroscience
In Molecular Biology
In Neurology
Citations in the corpus
- Mouse and rat BDNF gene structure and expression revisited (2006, background): “Alterations in BDNF expression in specific neuron subpopulations contribute to various pathologies, including depression, epilepsy, and Alzheimer’s, Huntington’s, and Parkinson’s diseases (Bibel and Barde, 2000; Murer et al., 2001; Binder and Scharfman, 2004; Castren, 2004; Cattaneo et al., 2005; Ru”
- Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “Huntingtin may have anti-apoptotic properties of the protein as well as the control of brain-derived neurotrophic factor production, vesicular transport, neuronal gene transcription and synaptic transmission (Cattaneo et al., 2005).”
- Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “At the same time, it also impairs the ability of normal huntingtin protein to exert molecular activities that are fundamental for the survival and functioning of the neurons that predominantly degenerate in the disease (99, 668).”
- Prion-like transmission of protein aggregates in neurodegenerative diseases (2010, background): “Its normal functions are not fully understood; it has been implicated in anti-apoptosis, neuronal gene transcription, synaptic function and vesicle and axonal transpor”
- The Role of MicroRNAs in Human Diseases (2010, background): “The manifestations of HD include cognitive defects and motor control impairment which lead to neuronal dysfunction characterized by progressive loss of cortical and striatal neurons ((142)).”