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In addition, treatment with IGF-1 peptide increases brain weight of the mutant mice. Multiple measurements support the hypothesis that RTT results from a deficit in synaptic maturation in the brain: MeCP2 mutant mice have sparse dendritic spines and reduced PSD-95 in motor cortex pyramidal neurons, reduced synaptic amplitude in the same neurons, and protracted cortical plasticity in vivo. Treatment with IGF-1 peptide partially restores spine density and synaptic amplitude, increases PSD-95, and stabilizes cortical plasticity to wild-type levels. Our results thus strongly suggest IGF-1 as a candidate for pharmacological treatment of RTT and potentially of other CNS disorders caused by delayed synapse maturation.<\/jats:p>","DOI":"10.1073\/pnas.0812394106","type":"journal-article","created":{"date-parts":[[2009,2,11]],"date-time":"2009-02-11T16:09:25Z","timestamp":1234368565000},"page":"2029-2034","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":520,"title":["Partial reversal of Rett Syndrome-like symptoms in MeCP2 mutant mice"],"prefix":"10.1073","volume":"106","author":[{"given":"Daniela","family":"Tropea","sequence":"first","affiliation":[{"name":"Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emanuela","family":"Giacometti","sequence":"additional","affiliation":[{"name":"Whitehead Institute for Biomedical Research, Cambridge, MA 02142; 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