The disease progression of Mecp2 mutant mice is affected by the level of BDNF expression.

By Q. Chang, G. Khare, Vardhan S Dani, Sacha B. Nelson, R. Jaenisch. Neuron, 2006

614 citations recorded by the source corpus.

Subfields: Cell Biology, Cognitive Neuroscience, Genetics

View Paper: https://www.semanticscholar.org/paper/9c8a7b2581381e7cfdc0592ca67562dbeef7375f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. H. Zoghbi
2. Mark F. Bear
3. L. Reichardt

In Cognitive Neuroscience

1. Mark F. Bear
2. H. Zoghbi
3. L. Monteggia
4. Thomas Bourgeron

In Genetics

1. Mark F. Bear
2. H. Zoghbi
3. G. Fan
4. Lisa D. Moore
5. Thuc M. Le
6. Thomas Bourgeron

Citations in the corpus

• Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “Conversely, overexpression of BDNF in MeCP2null mice delays the onset of RTT-associated features (Chang et al., 2006), further suggesting a link between alterations in BDNF levels and MeCP2.”
• The story of Rett syndrome: from clinic to neurobiology. (2007, neutral): “…in response to neuronal activity, the reduced cortical activity in Mecp2 null mice is expected to negatively affect Bdnf expression, hence masking the expected upregulation that would normally result from loss of repression in resting cortical neurons that lack MeCP2 (Chang et al., 2006).”
• DNA Methylation and Its Basic Function (2013, background): “The overexpression of BDNF in postmitotic neurons of MeCP2 mutant mice ameliorates their phenotype, suggesting that MeCP2 is critical for regulating the expression of genes like BDNF that are regulated by neuronal activity and essential for normal cognitive function (Chang et al, 2006).”
• Rett Syndrome and Fragile X Syndrome: Different Etiology With Common Molecular Dysfunctions (2021, background): “Brain derived neurotrophic factor level is deficient in Mecp2 KO mouse brain and, consistently, its overexpression has been shown to reverse some RTT phenotypes (Chang et al., 2006).”
• Neurotrophin-regulated signalling pathways (2006, background): “Although many of the cis elements and transcription factors involved in neurotrophin gene expression are being identified, there is no tissue or cell type in which these interactions are completely characterized (Lei et al. 2005; Chang et al. 2006).”
• GDNF, NGF and BDNF as therapeutic options for neurodegeneration. (2013, background): “BDNF overexpression increased lifespan and rescued locomotor activity (Chang et al., 2006).”
• Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, methodology): “The reductions of BDNF levels in Mecp2 -null mice coupled with the amelioration of phenotypes when BDNF is used exogenously or genetically (Chang et al. 2006; Kline et al. 2010) raise the possibility that drugs that enhance BDNF signaling might rescue RTT phenotypes.”