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- W2087367348 abstract "Mutations in the X-linked MECP2 gene are the primary cause of the severe autism spectrum disorder RTT (Rett syndrome). Deletion of Mecp2 in mice recapitulates many of the overt neurological features seen in humans, and the delayed onset of symptoms is accompanied by deficits in neuronal morphology and synaptic physiology. Recent evidence suggests that reactivation of endogenous Mecp2 in young and adult mice can reverse aspects of RTT-like pathology. In the current perspective, we discuss these findings as well as other genetic, pharmacological and environmental interventions that attempt phenotypic rescue in RTT. We believe these studies provide valuable insights into the tractability of RTT and related conditions and are useful pointers for the development of future therapeutic strategies." @default.
- W2087367348 created "2016-06-24" @default.
- W2087367348 creator A5000905868 @default.
- W2087367348 creator A5017860049 @default.
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- W2087367348 date "2010-03-22" @default.
- W2087367348 modified "2023-10-15" @default.
- W2087367348 title "Reversibility of functional deficits in experimental models of Rett syndrome" @default.
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- W2087367348 doi "https://doi.org/10.1042/bst0380498" @default.
- W2087367348 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20298210" @default.
- W2087367348 hasPublicationYear "2010" @default.
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