<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Custodio RJP</submitter><funding>National Research Foundation of Korea</funding><pagination>1101</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8452653</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4(1)</volume><pubmed_abstract>Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder, potentially with a biological basis; however, its exact cause remains unknown. Thyroid hormone (TH) abnormalities are more prevalent in patients with ADHD than in the general population, indicating a shared pathogenetic mechanism for these conditions. Previously, we identified that overexpression of thyroid hormone-responsive protein (THRSP), a gene highly responsive to TH status, induced inattention in male mice. Herein, we sought to explore whether TH function in THRSP-overexpressing (THRSP OE) mice influences ADHD-like (inattention) behavior. We now confirm that THRSP overexpression in male mice reproduces behavioral features of ADHD, including sustained inattention and memory impairment, accompanied by ex</pubmed_abstract><journal>Communications biology</journal><pubmed_title>Low striatal T3 is implicated in inattention and memory impairment in an ADHD mouse model overexpressing thyroid hormone-responsive protein.</pubmed_title><pmcid>PMC8452653</pmcid><funding_grant_id>2016R1D1A1B02010387; 2020M3E5D9080791</funding_grant_id><pubmed_authors>Sayson LV</pubmed_authors><pubmed_authors>Ortiz DM</pubmed_authors><pubmed_authors>Kim HJ</pubmed_authors><pubmed_authors>Cheong JH</pubmed_authors><pubmed_authors>Custodio RJP</pubmed_authors><pubmed_authors>Kim BN</pubmed_authors><pubmed_authors>Lee HJ</pubmed_authors><pubmed_authors>Kim M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Low striatal T3 is implicated in inattention and memory impairment in an ADHD mouse model overexpressing thyroid hormone-responsive protein.</name><description>Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder, potentially with a biological basis; however, its exact cause remains unknown. Thyroid hormone (TH) abnormalities are more prevalent in patients with ADHD than in the general population, indicating a shared pathogenetic mechanism for these conditions. Previously, we identified that overexpression of thyroid hormone-responsive protein (THRSP), a gene highly responsive to TH status, induced inattention in male mice. Herein, we sought to explore whether TH function in THRSP-overexpressing (THRSP OE) mice influences ADHD-like (inattention) behavior. We now confirm that THRSP overexpression in male mice reproduces behavioral features of ADHD, including sustained inattention and memory impairment, accompanied by ex</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2026-06-12T04:02:56.41Z</modification><creation>2022-02-11T11:47:05.805Z</creation></dates><accession>S-EPMC8452653</accession><cross_references><pubmed>34545202</pubmed><doi>10.1038/s42003-021-02633-w</doi></cross_references></HashMap>