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Insulin-like growth factor-1 rescues synaptic and motor deficits in a mouse model of autism and developmental delay / Ozlem BOZDAGI in Molecular Autism, (April 2013)
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Titre : Insulin-like growth factor-1 rescues synaptic and motor deficits in a mouse model of autism and developmental delay Type de document : Texte imprimé et/ou numérique Auteurs : Ozlem BOZDAGI, Auteur ; Teresa TAVASSOLI, Auteur ; Joseph D. BUXBAUM, Auteur Année de publication : 2013 Article en page(s) : 4 p. Langues : Anglais (eng) Mots-clés : Pharmacotherapy Personalized medicine Individualized medicine 22q13 deletion syndrome Phelan-McDermid syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND:Haploinsufficiency of SHANK3, due to either hemizygous gene deletion (termed 22q13 deletion syndrome or Phelan-McDermid syndrome) or to gene mutation, accounts for about 0.5% of the cases of autism spectrum disorder (ASD) and/or developmental delay, and there is evidence for a wider role for SHANK3 and glutamate signaling abnormalities in ASD and related conditions. Therapeutic approaches that reverse deficits in SHANK3-haploinsufficiency may therefore be broadly beneficial in ASD and in developmental delay.FINDINGS:We observed that daily intraperitoneal injections of human insulin-like growth factor 1 (IGF-1) over a 2-week period reversed deficits in hippocampal alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) signaling, long-term potentiation (LTP), and motor performance that we had previously reported in Shank3-deficient mice. Positive effects were observed with an IGF-1 peptide derivative as well.CONCLUSIONS:We observed significant beneficial effects of IGF-1 in a mouse model of ASD and of developmental delay. Studies in mouse and human neuronal models of Rett syndrome also show benefits with IGF-1, raising the possibility that this compound may have benefits broadly in ASD and related conditions, even with differing molecular etiology. Given the extensive safety data for IGF-1 in children with short stature due to primary IGF-1 deficiency, IGF-1 is an attractive candidate for controlled clinical trials in SHANK3-deficiency and in ASD. En ligne : http://dx.doi.org/10.1186/2040-2392-4-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202
in Molecular Autism > (April 2013) . - 4 p.[article] Insulin-like growth factor-1 rescues synaptic and motor deficits in a mouse model of autism and developmental delay [Texte imprimé et/ou numérique] / Ozlem BOZDAGI, Auteur ; Teresa TAVASSOLI, Auteur ; Joseph D. BUXBAUM, Auteur . - 2013 . - 4 p.
Langues : Anglais (eng)
in Molecular Autism > (April 2013) . - 4 p.
Mots-clés : Pharmacotherapy Personalized medicine Individualized medicine 22q13 deletion syndrome Phelan-McDermid syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND:Haploinsufficiency of SHANK3, due to either hemizygous gene deletion (termed 22q13 deletion syndrome or Phelan-McDermid syndrome) or to gene mutation, accounts for about 0.5% of the cases of autism spectrum disorder (ASD) and/or developmental delay, and there is evidence for a wider role for SHANK3 and glutamate signaling abnormalities in ASD and related conditions. Therapeutic approaches that reverse deficits in SHANK3-haploinsufficiency may therefore be broadly beneficial in ASD and in developmental delay.FINDINGS:We observed that daily intraperitoneal injections of human insulin-like growth factor 1 (IGF-1) over a 2-week period reversed deficits in hippocampal alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) signaling, long-term potentiation (LTP), and motor performance that we had previously reported in Shank3-deficient mice. Positive effects were observed with an IGF-1 peptide derivative as well.CONCLUSIONS:We observed significant beneficial effects of IGF-1 in a mouse model of ASD and of developmental delay. Studies in mouse and human neuronal models of Rett syndrome also show benefits with IGF-1, raising the possibility that this compound may have benefits broadly in ASD and related conditions, even with differing molecular etiology. Given the extensive safety data for IGF-1 in children with short stature due to primary IGF-1 deficiency, IGF-1 is an attractive candidate for controlled clinical trials in SHANK3-deficiency and in ASD. En ligne : http://dx.doi.org/10.1186/2040-2392-4-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202