Insulin-like growth factor-1 rescues synaptic and motor deficits in a mouse model of autism and developmental delay

Molecular Autism - Tập 4 - Trang 1-4 - 2013
Ozlem Bozdagi1,2, Teresa Tavassoli1,2, Joseph D Buxbaum1,2,3,4,5,6
1Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, USA
2Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, USA
3Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, USA
4Department of Genetics and Genomics Sciences, Icahn School of Medicine at Mount Sinai, New York, USA
5Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, USA
6Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, USA

Tóm tắt

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. We observed that daily intraperitoneal injections of human insulin-like growth factor 1 (IGF-1) over a 2-week period reversed deficits in hippocampal α-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. 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.

Tài liệu tham khảo

Boeckers TM, Bockmann J, Kreutz MR, Gundelfinger ED: ProSAP/Shank proteins - a family of higher order organizing molecules of the postsynaptic density with an emerging role in human neurological disease. J Neurochem. 2002, 81 (5): 903-910. 10.1046/j.1471-4159.2002.00931.x. Abrahams BS, Geschwind DH: Advances in autism genetics: on the threshold of a new neurobiology. Nat Rev Genet. 2008, 9 (5): 341-355. 10.1038/nrg2346. Sakai Y, Shaw CA, Dawson BC, Dugas DV, Al-Mohtaseb Z, Hill DE: Protein interactome reveals converging molecular pathways among autism disorders. Sci Transl Med. 2011, 3 (86): 86ra49-10.1126/scitranslmed.3002166. Darnell JC, Van Driesche SJ, Zhang C, Hung KY, Mele A, Fraser CE: FMRP stalls ribosomal translocation on mRNAs linked to synaptic function and autism. Cell. 2011, 146 (2): 247-261. 10.1016/j.cell.2011.06.013. Bozdagi O, Sakurai T, Papapetrou D, Wang X, Dickstein DL, Takahashi N: Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication. Mol Aut. 2010, 1 (1): 15-10.1186/2040-2392-1-15. Wang X, McCoy PA, Rodriguiz RM, Pan Y, Je HS, Roberts AC: Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3. Hum Mol Genet. 2011, 20 (15): 3093-3108. 10.1093/hmg/ddr212. Yang M, Bozdagi O, Scattoni ML, Wohr M, Roullet FI, Katz AM: Reduced excitatory neurotransmission and mild autism-relevant phenotypes in adolescent Shank3 null mutant mice. J Neurosci. 2012, 32 (19): 6525-6541. 10.1523/JNEUROSCI.6107-11.2012. Nishijima T, Piriz J, Duflot S, Fernandez AM, Gaitan G, Gomez-Pinedo U: Neuronal activity drives localized blood–brain-barrier transport of serum insulin-like growth factor-I into the CNS. Neuron. 2010, 67 (5): 834-846. 10.1016/j.neuron.2010.08.007. O’Kusky JR, Ye P, D’Ercole AJ: Insulin-like growth factor-I promotes neurogenesis and synaptogenesis in the hippocampal dentate gyrus during postnatal development. J Neurosci. 2000, 20 (22): 8435-8442. Shi L, Linville MC, Tucker EW, Sonntag WE, Brunso-Bechtold JK: Differential effects of aging and insulin-like growth factor-1 on synapses in CA1 of rat hippocampus. Cereb Cortex. 2005, 15 (5): 571-577. Tropea D, Giacometti E, Wilson NR, Beard C, McCurry C, Fu DD: Partial reversal of Rett syndrome-like symptoms in MeCP2 mutant mice. Proc Natl Acad Sci USA. 2009, 106 (6): 2029-2034. 10.1073/pnas.0812394106. Moessner R, Marshall CR, Sutcliffe JS, Skaug J, Pinto D, Vincent J: Contribution of SHANK3 mutations to autism spectrum disorder. Am J Hum Genet. 2007, 81 (6): 1289-1297. 10.1086/522590. Hamdan FF, Gauthier J, Araki Y, Lin DT, Yoshizawa Y, Higashi K: Excess of de novo deleterious mutations in genes associated with glutamatergic systems in nonsyndromic intellectual disability. Am J Hum Genet. 2011, 88 (3): 306-316. 10.1016/j.ajhg.2011.02.001. Laumonnier F, Cuthbert PC, Grant SG: The role of neuronal complexes in human X-linked brain diseases. Am J Hum Genet. 2007, 80 (2): 205-220. 10.1086/511441. Marchetto MC, Carromeu C, Acab A, Yu D, Yeo GW, Mu Y: A model for neural development and treatment of Rett syndrome using human induced pluripotent stem cells. Cell. 2010, 143 (4): 527-539. 10.1016/j.cell.2010.10.016.