<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ma J</submitter><funding>National Natural Science Foundation of China</funding><funding>National key research and development program</funding><funding>4th Three-year Action Plan for Public Health of Shanghai</funding><funding>Shanghai Pujiang Program</funding><funding>Shanghai Key Laboratory of Psychotic Disorders</funding><pagination>1780-1790</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8977635</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(10)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Catechol-O-methyltransferase (COMT) contributes to the control of synaptic dopamine (DA) transmission by catalyzing DA degradation in the presynaptic space. The COMT Val158Met polymorphism (rs4680) substantially alters enzymatic activity and consequently synaptic DA concentration in the prefrontal cortex and hippocampus. The COMT genotype could, therefore, exert a major influence on antipsychotic treatment response as many of these agents also target dopaminergic transmission.&lt;h4>Objective&lt;/h4>The present meta-analysis aimed to test a putative relationship between the COMT Val158Met polymorphism and antipsychotic response across different populations and antipsychotic types.&lt;h4>Methods&lt;/h4>Searches of PubMed, Web of Science, EMBASE, OVID, Google Scholar, and Baidu Schola</pubmed_abstract><journal>Current neuropharmacology</journal><pubmed_title>Association Between the COMT Val158Met Polymorphism and Antipsychotic Efficacy in Schizophrenia: An Updated Meta-Analysis.</pubmed_title><pmcid>PMC8977635</pmcid><funding_grant_id>81773818, 81273596, 30900799, 81671326</funding_grant_id><funding_grant_id>81773818</funding_grant_id><funding_grant_id>2016YFC0906400</funding_grant_id><funding_grant_id>2016YFC0905002</funding_grant_id><funding_grant_id>17PJD020</funding_grant_id><funding_grant_id>15GWZK0101</funding_grant_id><funding_grant_id>2016YFC1200200</funding_grant_id><funding_grant_id>2016YFC0905000</funding_grant_id><funding_grant_id>81671326</funding_grant_id><funding_grant_id>81273596</funding_grant_id><funding_grant_id>2016YFC0905000, 2016YFC0905002, 2016YFC1200200, 2016YFC0906400</funding_grant_id><funding_grant_id>13DZ2260500</funding_grant_id><funding_grant_id>30900799</funding_grant_id><pubmed_authors>Shen L</pubmed_authors><pubmed_authors>Zhao M</pubmed_authors><pubmed_authors>Huai C</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Zhang N</pubmed_authors><pubmed_authors>Ma J</pubmed_authors><pubmed_authors>Zhou W</pubmed_authors><pubmed_authors>He L</pubmed_authors><pubmed_authors>Li M</pubmed_authors><pubmed_authors>Wu H</pubmed_authors><pubmed_authors>Qin S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association Between the COMT Val158Met Polymorphism and Antipsychotic Efficacy in Schizophrenia: An Updated Meta-Analysis.</name><description>&lt;h4>Background&lt;/h4>Catechol-O-methyltransferase (COMT) contributes to the control of synaptic dopamine (DA) transmission by catalyzing DA degradation in the presynaptic space. The COMT Val158Met polymorphism (rs4680) substantially alters enzymatic activity and consequently synaptic DA concentration in the prefrontal cortex and hippocampus. The COMT genotype could, therefore, exert a major influence on antipsychotic treatment response as many of these agents also target dopaminergic transmission.&lt;h4>Objective&lt;/h4>The present meta-analysis aimed to test a putative relationship between the COMT Val158Met polymorphism and antipsychotic response across different populations and antipsychotic types.&lt;h4>Methods&lt;/h4>Searches of PubMed, Web of Science, EMBASE, OVID, Google Scholar, and Baidu Schola</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-05-09T20:11:03.54Z</modification><creation>2025-02-19T00:56:40.718Z</creation></dates><accession>S-EPMC8977635</accession><cross_references><pubmed>33100205</pubmed><doi>10.2174/1570159X18666201023154049</doi></cross_references></HashMap>