Pharmacological interference with the glucocorticoid system influences symptoms and lifespan in a mouse model of Rett syndrome.
Research output: Contribution to journal › Article
Rett syndrome (RTT) is caused by loss-of-function mutations in the X-linked gene MECP2 coding for methyl CpG-binding protein 2 (MeCP2). This protein can act as transcriptional repressor and we showed in a previous study that glucocorticoid-inducible genes are up-regulated in a RTT mouse model and that these genes are direct MeCP2 targets. Here, we report that pharmacological intervention with the glucocorticoid system has an impact on the symptoms and lifespan in a RTT mouse model. Our data support a functional implication of the stress hormone system in RTT and suggest this hormone system as potential therapeutic target.
|Research areas and keywords||
Subject classification (UKÄ) – MANDATORY
|Journal||Human Molecular Genetics|
|Publication status||Published - 2012|
Related research output
Sebastian Braun, 2012, 105 p.
Research output: Thesis › Doctoral Thesis (compilation)