<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wan Y</submitter><funding>Projects of the Shanghai Committee of Science and Technology</funding><funding>Projects of National Science Foundation of China</funding><funding>Medical Engineering Cross Research Fund of Shanghai Jiao Tong University</funding><funding>Medical Engineering Cross Research Fund of University of Shanghai for Science and Technology</funding><funding>Shanghai Demonstration Project of Cooperative Diagnosis and Treatment for Major Difficult Diseases with integrative modern and traditional Chinese medicine</funding><funding>National Key Research and Development Program of China</funding><funding>Innovative research team of high-level local universities in Shanghai</funding><pagination>11572-11580</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12367974</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>62(9)</volume><pubmed_abstract>Levodopa induced dyskinesia (LID) is a serious side effect of levodopa treatment in Parkinson's disease (PD), with limited interventions. Understanding the genetic impact on LID would help inform future intervention studies. We performed integrative genomic analysis approaches to identify the genetic determinants of LID in a Chinese multi-center prospective, observational PD cohort. In this cohort, 46 of 315 PD patients developed LID during 2.5 years of follow-up. First, we performed a genome-wide association study (GWAS) in this cohort, followed by a meta-analysis integrating our GWAS summary data with additional data of European ancestry. Both GWAS analyses identified the Bromodomain Containing 3 (BRD3) as a LID susceptibility gene (P &lt; 5 × 10&lt;sup>-8&lt;/sup>); however, the genetic variants</pubmed_abstract><journal>Molecular neurobiology</journal><pubmed_title>Integrative Approaches Identify Genetic Determinants of Levodopa Induced Dyskinesia.</pubmed_title><pmcid>PMC12367974</pmcid><funding_grant_id>SHSMU-ZDCX20211901</funding_grant_id><funding_grant_id>2017YFC1310300</funding_grant_id><funding_grant_id>22Y11904100</funding_grant_id><funding_grant_id>81974173</funding_grant_id><funding_grant_id>ZY(2021-2023)-0207-01-03</funding_grant_id><funding_grant_id>YG2023ZD12</funding_grant_id><funding_grant_id>2023GD-XH06Z</funding_grant_id><pubmed_authors>Shao J</pubmed_authors><pubmed_authors>Zhang K</pubmed_authors><pubmed_authors>Wan Y</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Ye M</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Luo W</pubmed_authors><pubmed_authors>Guo D</pubmed_authors><pubmed_authors>Xie A</pubmed_authors><pubmed_authors>Rong L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Integrative Approaches Identify Genetic Determinants of Levodopa Induced Dyskinesia.</name><description>Levodopa induced dyskinesia (LID) is a serious side effect of levodopa treatment in Parkinson's disease (PD), with limited interventions. Understanding the genetic impact on LID would help inform future intervention studies. We performed integrative genomic analysis approaches to identify the genetic determinants of LID in a Chinese multi-center prospective, observational PD cohort. In this cohort, 46 of 315 PD patients developed LID during 2.5 years of follow-up. First, we performed a genome-wide association study (GWAS) in this cohort, followed by a meta-analysis integrating our GWAS summary data with additional data of European ancestry. Both GWAS analyses identified the Bromodomain Containing 3 (BRD3) as a LID susceptibility gene (P &lt; 5 × 10&lt;sup>-8&lt;/sup>); however, the genetic variants</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-05-29T17:17:06.795Z</modification><creation>2026-04-08T05:25:11.189Z</creation></dates><accession>S-EPMC12367974</accession><cross_references><pubmed>40299300</pubmed><doi>10.1007/s12035-025-04930-5</doi></cross_references></HashMap>