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Dysregulation of mTOR signaling has been implicated in the pathogenesis of certain types of ASD, and inhibition of mTOR by rapamycin has been demonstrated to be an effective therapeutics for impaired social interaction in <jats:italic>Tsc1<\/jats:italic>+\/<jats:italic>\u2212<\/jats:italic>, Tsc2+\/<jats:italic>\u2212<\/jats:italic>, <jats:italic>Pten<\/jats:italic>\u2212\/\u2212 mice and valproic acid-induced ASD animal models. However, it is still unknown if dysregulation of mTOR signaling is responsible for the ASD-related deficit caused by other genes mutations. <jats:italic>Contactin associated protein-like 2<\/jats:italic> (<jats:italic>CNTNAP2<\/jats:italic>) is the first widely replicated autism-predisposition gene. Mice deficient in <jats:italic>Cntnap2<\/jats:italic> (<jats:italic>Cntnap2<\/jats:italic>\u2212\/\u2212 mice) show core ASD-like phenotypes, and have been demonstrated as a validated model for ASD-relevant drug discovery. In this study, we found hyperactive Akt-mTOR signaling in the hippocampus of <jats:italic>Cntnap2<\/jats:italic>\u2212\/\u2212 mice with RNA sequencing followed with biochemical analysis. Treatment with Akt inhibitor LY294002 or mTOR inhibitor rapamycin rescued the social deficit, but had no effect on hyperactivity and repetitive behavior\/restricted behavior in <jats:italic>Cntnap2<\/jats:italic>\u2212\/\u2212 mice. We further showed that the effect of LY294002 and rapamycin on social behaviors is reversible. Our results thus identified hyperactive Akt-mTOR signaling pathway as a therapeutic target for abnormal social behavior in patients with dysfunction of CNTNAP2.<\/jats:p>","DOI":"10.1038\/s41598-019-39434-5","type":"journal-article","created":{"date-parts":[[2019,2,28]],"date-time":"2019-02-28T11:05:03Z","timestamp":1551351903000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":68,"title":["Suppression of Akt-mTOR pathway rescued the social behavior in Cntnap2-deficient mice"],"prefix":"10.1038","volume":"9","author":[{"given":"Xiaoliang","family":"Xing","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunyang","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beibei","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianfeng","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengmao","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kun","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia-Da","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,2,28]]},"reference":[{"key":"39434_CR1","doi-asserted-by":"publisher","first-page":"f3591","DOI":"10.1136\/bmj.f3591","volume":"346","author":"B Roehr","year":"2013","unstructured":"Roehr, B. 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