<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Smith GS</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>National Center for Research Resources</funding><funding>NCATS NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Institute of Mental Health</funding><funding>National Institutes of Health</funding><funding>National Institute on Aging</funding><pagination>108447</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8716112</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>194</volume><pubmed_abstract>Patients with late-life depression (LLD) have a more variable response to pharmacotherapy relative to patients with mid-life depression. Degeneration of the serotonergic system and lower occupancy of the initial target for antidepressant medications, the serotonin transporter (5-HTT), may contribute to variability in treatment response. The focus of this study was to test the hypotheses that lower cortical and limbic serotonin transporter (5-HTT) availability in LLD patients relative to controls and less 5-HTT occupancy by antidepressant medications would be associated with less improvement in mood and cognition with treatment in LLD patients. Twenty LLD patients meeting DSM-IV criteria for a current major depressive episode and 20 non-depressed controls underwent clinical and neuropsychol</pubmed_abstract><journal>Neuropharmacology</journal><pubmed_title>Molecular imaging of the serotonin transporter availability and occupancy by antidepressant treatment in late-life depression.</pubmed_title><pmcid>PMC8716112</pmcid><funding_grant_id>MH064823</funding_grant_id><funding_grant_id>R01 AG059390</funding_grant_id><funding_grant_id>UL1 TR003098</funding_grant_id><funding_grant_id>R01 AG041633</funding_grant_id><funding_grant_id>UL1 TR001079</funding_grant_id><funding_grant_id>AG059390</funding_grant_id><funding_grant_id>R01 MH064823</funding_grant_id><funding_grant_id>AG038893</funding_grant_id><funding_grant_id>AG041633</funding_grant_id><funding_grant_id>MH086881</funding_grant_id><funding_grant_id>R01 MH086881</funding_grant_id><funding_grant_id>R01 AG038893</funding_grant_id><pubmed_authors>Smith GS</pubmed_authors><pubmed_authors>Joo JH</pubmed_authors><pubmed_authors>Mathews WB</pubmed_authors><pubmed_authors>Dannals RF</pubmed_authors><pubmed_authors>Nandi A</pubmed_authors><pubmed_authors>Holt DP</pubmed_authors><pubmed_authors>Bigos KL</pubmed_authors><pubmed_authors>Kraut M</pubmed_authors><pubmed_authors>Kuwabara H</pubmed_authors><pubmed_authors>Workman CI</pubmed_authors><pubmed_authors>Hall AW</pubmed_authors><pubmed_authors>Brasic J</pubmed_authors><pubmed_authors>Savonenko A</pubmed_authors><pubmed_authors>Gould NF</pubmed_authors><pubmed_authors>Nassery N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Molecular imaging of the serotonin transporter availability and occupancy by antidepressant treatment in late-life depression.</name><description>Patients with late-life depression (LLD) have a more variable response to pharmacotherapy relative to patients with mid-life depression. Degeneration of the serotonergic system and lower occupancy of the initial target for antidepressant medications, the serotonin transporter (5-HTT), may contribute to variability in treatment response. The focus of this study was to test the hypotheses that lower cortical and limbic serotonin transporter (5-HTT) availability in LLD patients relative to controls and less 5-HTT occupancy by antidepressant medications would be associated with less improvement in mood and cognition with treatment in LLD patients. Twenty LLD patients meeting DSM-IV criteria for a current major depressive episode and 20 non-depressed controls underwent clinical and neuropsychol</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-04T19:40:32.776Z</modification><creation>2025-04-04T19:40:32.776Z</creation></dates><accession>S-EPMC8716112</accession><cross_references><pubmed>33450276</pubmed><doi>10.1016/j.neuropharm.2021.108447</doi></cross_references></HashMap>