<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lawrence KE</submitter><funding>NCRR NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Institute of Mental Health</funding><funding>NINDS NIH HHS</funding><funding>NIH HHS</funding><pagination>378-387</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8967090</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>145(1)</volume><pubmed_abstract>The biological mechanisms underlying the greater prevalence of autism spectrum disorder in males than females remain poorly understood. One hypothesis posits that this female protective effect arises from genetic load for autism spectrum disorder differentially impacting male and female brains. To test this hypothesis, we investigated the impact of cumulative genetic risk for autism spectrum disorder on functional brain connectivity in a balanced sample of boys and girls with autism spectrum disorder and typically developing boys and girls (127 youth, ages 8-17). Brain connectivity analyses focused on the salience network, a core intrinsic functional connectivity network which has previously been implicated in autism spectrum disorder. The effects of polygenic risk on salience network func</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Impact of autism genetic risk on brain connectivity: a mechanism for the female protective effect.</pubmed_title><pmcid>PMC8967090</pmcid><funding_grant_id>R01MH100028</funding_grant_id><funding_grant_id>T32 NS048004</funding_grant_id><funding_grant_id>F31 MH110140</funding_grant_id><funding_grant_id>R01 MH100028</funding_grant_id><funding_grant_id>C06 RR012169</funding_grant_id><funding_grant_id>S10 OD011939</funding_grant_id><funding_grant_id>C06 RR015431</funding_grant_id><funding_grant_id>F32 MH105167</funding_grant_id><funding_grant_id>R01 MH117982</funding_grant_id><funding_grant_id>K00 MH119663</funding_grant_id><pubmed_authors>GENDAAR Consortium</pubmed_authors><pubmed_authors>MacDonnell E</pubmed_authors><pubmed_authors>Naples A</pubmed_authors><pubmed_authors>Patterson G</pubmed_authors><pubmed_authors>Bernier RA</pubmed_authors><pubmed_authors>Kresse A</pubmed_authors><pubmed_authors>McDonald N</pubmed_authors><pubmed_authors>Bookheimer SY</pubmed_authors><pubmed_authors>Depedro-Mercier D</pubmed_authors><pubmed_authors>Jacokes Z</pubmed_authors><pubmed_authors>Okada NJ</pubmed_authors><pubmed_authors>Guilford D</pubmed_authors><pubmed_authors>Libsack E</pubmed_authors><pubmed_authors>Tsapelas H</pubmed_authors><pubmed_authors>Pelphrey KA</pubmed_authors><pubmed_authors>Neuhaus E</pubmed_authors><pubmed_authors>Hernandez LM</pubmed_authors><pubmed_authors>Wolf J</pubmed_authors><pubmed_authors>Dapretto M</pubmed_authors><pubmed_authors>Ankenman K</pubmed_authors><pubmed_authors>Ventola P</pubmed_authors><pubmed_authors>Geschwind DH</pubmed_authors><pubmed_authors>Webb SJ</pubmed_authors><pubmed_authors>Van Horn JD</pubmed_authors><pubmed_authors>Sullivan CAW</pubmed_authors><pubmed_authors>Jung J</pubmed_authors><pubmed_authors>Lawrence KE</pubmed_authors><pubmed_authors>Gaab N</pubmed_authors><pubmed_authors>Keifer CM</pubmed_authors><pubmed_authors>McPartland JC</pubmed_authors><pubmed_authors>Jack A</pubmed_authors><pubmed_authors>Torgerson CM</pubmed_authors><pubmed_authors>Jeste S</pubmed_authors><pubmed_authors>Lowe JK</pubmed_authors><pubmed_authors>Welker O</pubmed_authors><pubmed_authors>Padgaonkar NT</pubmed_authors><pubmed_authors>Fuster E</pubmed_authors><pubmed_authors>Gupta AR</pubmed_authors><pubmed_authors>Aylward E</pubmed_authors><pubmed_authors>Nelson CA</pubmed_authors><pubmed_authors>Corrigan S</pubmed_authors><pubmed_authors>Hoekstra JN</pubmed_authors><pubmed_authors>Green SA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of autism genetic risk on brain connectivity: a mechanism for the female protective effect.</name><description>The biological mechanisms underlying the greater prevalence of autism spectrum disorder in males than females remain poorly understood. One hypothesis posits that this female protective effect arises from genetic load for autism spectrum disorder differentially impacting male and female brains. To test this hypothesis, we investigated the impact of cumulative genetic risk for autism spectrum disorder on functional brain connectivity in a balanced sample of boys and girls with autism spectrum disorder and typically developing boys and girls (127 youth, ages 8-17). Brain connectivity analyses focused on the salience network, a core intrinsic functional connectivity network which has previously been implicated in autism spectrum disorder. The effects of polygenic risk on salience network func</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-06T23:23:31.04Z</modification><creation>2025-04-04T11:29:12.081Z</creation></dates><accession>S-EPMC8967090</accession><cross_references><pubmed>34050743</pubmed><doi>10.1093/brain/awab204</doi></cross_references></HashMap>