Loss of Huntingtin-Mediated BDNF Gene Transcription in Huntington's Disease

By C. Zuccato, A. Ciammola, D. Rigamonti, B. Leavitt, Donato Goffredo, L. Conti, M. MacDonald, R. Friedlander, V. Silani, Michael R. Hayden and 3 more. Science, 2001

1,397 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a5232698225fc9f722c4bbb74761465662124298

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Citations in the corpus

GDNF, NGF and BDNF as therapeutic options for neurodegeneration. (2013, background): “In fact BDNF cortical tissue levels may be reduced by up to 45% in HD (Ferrer et al., 2000; Zuccato et al., 2001); and support for the striatal neurones is worsened by impaired huntingtin-mediated BDNF transport from the cortex (Gauthier et al., 2004).”
Brain-derived neurotrophic factor. (2004, background): “In humans, a valine to methionine polymorphism at the 50 pro-region of the human BDNF protein was found to be associated with poorer episodic memory; in vitro, neurons transfected with met-BDNF-GFP exhib- ited reduced depolarization-induced BDNF secretion (Egan et al., 2003).”
Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila. (2003, neutral): “Indeed, we found thatmouse HD brains (Zuccato et al., 2001).”
Diseases of Unstable Repeat Expansion: Mechanisms and Common Principles (2005, background): “Although the expansion might interfere with the normal function of the host protei”
Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines (2002, background): “It is widely believed that in HD, Htt gains an additional, toxic function, but some loss of normal Htt function may also be important in pathogenesi”
Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes (2003, background): “We previously reported that wild-type but not mutant huntingtin stimulates transcription of the gene encoding brain-derived neurotrophic factor ( BDNF ; ref”
Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, positive): “Diseases associated with some perturbation of BDNF signaling are diverse: epilepsy (He et al., 2004); mood disorders (Neves-Pereira et al., 2002; Sklar et al., 2002; Schumacher et al., 2005; Strauss et al., 2005), neurodegenerative diseases such Huntington's Disease (Zuccato et al., 2001; Zuccato et”
The Brain-Derived Neurotrophic Factor val66met Polymorphism and Variation in Human Cortical Morphology (2004, neutral): “, 2004), in which it has been implicated in various psychiatric and neurological diseases (Zuccato et al., 2001; Bimonte-Nelson et al., 2003; Weickert et al., 2003; Baquet et al., 2004).”
Brain-derived neurotrophic factor and its clinical implications (2015, background): “It was reported [119] that wild-type huntingtin up-regulates transcription of BDNF, a pro-survival factor produced by cortical neurons that is necessary for survival of striatal neurons in the brain.”
Ageing and neuronal vulnerability (2006, background): “Studies of patients with HD and huntingtin-mutant mice have revealed reduced levels of BDNF in the striatum and corte”
Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice (2008, background): “, 2004), and has previously been implicated in HD pathogenesis (Zuccato et al., 2001; Gauthier et al., 2004).”
Selective striatal neuronal loss in a YAC128 mouse model of Huntington disease. (2003, background): “These mice have helped elucidate different pathways involved in the pathogenesis of HD including increased susceptibility to excitotoxic cell death of neurons with mutant huntingtin (11–13), the discovery of decreased BDNF production in HD (14), the presence of mitochondrial dysfunction (15), and th”
Persistence of long-term memory storage requires a late protein synthesis- and BDNF- dependent phase in the hippocampus. (2007, neutral): “…Pezawas et al., 2004; Qiao et al., 1998; Rattiner et al., 2004; Tokuyama et al., 2000), and they have also been implicated in brain disorders that involve cognitive decline (Howells et al., 2000; Peng et al., 2005; Phillips et al., 1991; Saura et al., 2004; Tong et al., 2004; Zuccato et al., 2001).”