PubMed:25627160 / 1394-1900 JSONTXT

{"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T4","span":{"begin":0,"end":506},"obj":"CONCLUSIONS"}],"text":"In contrast to some monogenic disorders with high rates of autism, our data demonstrate down-regulation of the Akt/mTOR pathway, specifically via p70S6K/eIF4B, in idiopathic autism. These findings suggest that disruption of this pathway in either direction is widespread in autism and can have adverse consequences for synaptic function. The use of valproic acid, a histone deacetylase inhibitor, in rats successfully modeled these changes, implicating an epigenetic mechanism in these pathway disruptions."}

{"project":"NEUROSES","denotations":[{"id":"T21","span":{"begin":328,"end":336},"obj":"PATO_0000173"},{"id":"T36","span":{"begin":45,"end":49},"obj":"PATO_0000469"},{"id":"T37","span":{"begin":93,"end":103},"obj":"PATO_0000076"},{"id":"T38","span":{"begin":247,"end":256},"obj":"PATO_0000039"}],"text":"In contrast to some monogenic disorders with high rates of autism, our data demonstrate down-regulation of the Akt/mTOR pathway, specifically via p70S6K/eIF4B, in idiopathic autism. These findings suggest that disruption of this pathway in either direction is widespread in autism and can have adverse consequences for synaptic function. The use of valproic acid, a histone deacetylase inhibitor, in rats successfully modeled these changes, implicating an epigenetic mechanism in these pathway disruptions."}

{"project":"BLAH2015_Annotations_test_5","denotations":[{"id":"T29","span":{"begin":45,"end":49},"obj":"PATO_0000469"},{"id":"T30","span":{"begin":93,"end":103},"obj":"PATO_0000076"},{"id":"T31","span":{"begin":247,"end":256},"obj":"PATO_0000039"},{"id":"T14","span":{"begin":328,"end":336},"obj":"PATO_0000173"},{"id":"T9","span":{"begin":349,"end":362},"obj":"CHEBI_39867"},{"id":"T32","span":{"begin":366,"end":395},"obj":"CHEBI_61115"}],"text":"In contrast to some monogenic disorders with high rates of autism, our data demonstrate down-regulation of the Akt/mTOR pathway, specifically via p70S6K/eIF4B, in idiopathic autism. These findings suggest that disruption of this pathway in either direction is widespread in autism and can have adverse consequences for synaptic function. The use of valproic acid, a histone deacetylase inhibitor, in rats successfully modeled these changes, implicating an epigenetic mechanism in these pathway disruptions."}