期刊
JOURNAL OF NEUROSCIENCE
卷 38, 期 4, 页码 1015-1029出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2010-17.2017
关键词
autism spectrum disorder; insulin-like growth factor II receptor; insulin-like growth factor II; memory; mouse model; mTOR
资金
- [R37-MH065635]
- [R01-MH074736]
- [T32-MH019524]
- [F31-MH090636]
- NATIONAL INSTITUTE OF MENTAL HEALTH [T32MH087004, R01MH074736, T32MH019524, R37MH065635, F31MH090636] Funding Source: NIH RePORTER
Autism spectrum disorder (ASD) is a developmental disability characterized by impairments in social interaction and repetitive behavior, and is also associated with cognitive deficits. There is no current treatment that can ameliorate most of the ASD symptomatology; thus, identifying novel therapies is urgently needed. We used male BTBR T+ Itpr3(tf)/J (BTBR) mice, a model that reproduces most of the core behavioral phenotypes of ASD, to test the effects of systemic administration of insulin-like growth factor II (IGF-II), a polypeptide that crosses the blood-brain barrier and acts as a cognitive enhancer. We show that systemic IGF-II treatments reverse the typical defects in social interaction, cognitive/executive functions, and repetitive behaviors reflective of ASD-like phenotypes. In BTBR mice, IGF-II, via IGF-II receptor, but not via IGF-I receptor, reverses the abnormal levels of the AMPK-mTOR-S6K pathway and of active translation at synapses. Thus, IGF-II may represent a novel potential therapy for ASD.
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