Pharmacological interference with the glucocorticoid system influences symptoms and lifespan in a mouse model of Rett syndrome.

Sebastian Braun, Denise Kottwitz, Ulrike Nuber

Research output: Contribution to journalArticlepeer-review

Abstract

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.
Original languageEnglish
Pages (from-to)1673-1680
JournalHuman Molecular Genetics
Volume21
Issue number8
DOIs
Publication statusPublished - 2012

Subject classification (UKÄ)

  • Medical Genetics

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