ArticleSchizophrenia bulletin2016
Genome-Wide Association Study Suggested the PTPRD Polymorphisms Were Associated With Weight Gain Effects of Atypical Antipsychotic Medications.
Article in Schizophrenia bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Pharmacogenetic study of antipsychotic-induced lipid and BMI changes in Chinese schizophrenia patients: A Genome-Wide Association Study.Translational psychiatry · 2025Article
- Neurodevelopment Genes Encoding Olduvai Domains Link Myalgic Encephalomyelitis to Neuropsychiatric Disorders.Diagnostics (Basel, Switzerland) · 2025Article
- Genome-wide association study implicates lipid pathway dysfunction in antipsychotic-induced weight gain: multi-ancestry validation.Molecular psychiatry · 2024Article
- Clinical Utility and Implementation of Pharmacogenomics for the Personalisation of Antipsychotic Treatments.Pharmaceutics · 2024Review
- Prediction of treatment response to antipsychotic drugs for precision medicine approach to schizophrenia: randomized trials and multiomics analysis.Military Medical Research · 2023Article
- Identification of four novel loci associated with psychotropic drug-induced weight gain in a Swiss psychiatric longitudinal study: A GWAS analysis.Molecular psychiatry · 2023Article
- Mice lacking Ptprd exhibit deficits in goal-directed behavior and female-specific impairments in sensorimotor gating.PloS one · 2023Article
- Systems-Level Analysis of Genetic Variants Reveals Functional and Spatiotemporal Context in Treatment-resistant Schizophrenia.Molecular neurobiology · 2022Article
- Genome-wide association analyses of symptom severity among clozapine-treated patients with schizophrenia spectrum disorders.Translational psychiatry · 2022Article
- Functional genetic variants in the 3'UTR of PTPRD associated with the risk of gestational diabetes mellitus.Experimental and therapeutic medicine · 2021Article
- Association ofFrontiers in psychiatry · 2021Article
- The Burden of Antipsychotic-Induced Weight Gain and Metabolic Syndrome in Children.Frontiers in psychiatry · 2021Review
- Identification ofFrontiers in pharmacology · 2021Article
- A new genetic locus for antipsychotic-induced weight gain: A genome-wide study of first-episode psychosis patients using amisulpride (from the OPTiMiSE cohort).Journal of psychopharmacology (Oxford, England) · 2020Article
- Pharmacogenetics of Antipsychotic Drug Treatment: Update and Clinical Implications.Molecular neuropsychiatry · 2020Review
- Benefits and limitations of genome-wide association studies.Nature reviews. Genetics · 2019Review
- Pharmacogenetic Correlates of Antipsychotic-Induced Weight Gain in the Chinese Population.Neuroscience bulletin · 2019Review
- Effect of Metformin on Antipsychotic-Induced Metabolic Dysfunction: The Potential Role of Gut-Brain Axis.Frontiers in pharmacology · 2019Article
- Genetic validation study of protein tyrosine phosphatase receptor type D (PTPRD) gene variants and risk for antipsychotic-induced weight gain.Journal of neural transmission (Vienna, Austria : 1996) · 2019Article
- Weight Gain During Treatment of Bipolar Disorder (BD)-Facts and Therapeutic Options.Frontiers in nutrition · 2019Review
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Authors and funding
19 authors at 8 institutions in 2 countries.
Funding
Abstract
backgroundAntipsychotic-induced weight gain (AIWG) is a serious concern in therapy with antipsychotic medications. To identify single nucleotide polymorphisms (SNPs) associated with AIWG, we conducted a genome-wide association study (GWAS) for antipsychotic treatment.
methodsThe discovery cohort consisted of 534 patients with schizophrenia, who underwent 8-week treatment with antipsychotics and were genotyped using the Illumina Human 610-Quad BeadChip. The independent replication cohort consisted of 547 patients with schizophrenia, treated with similar antipsychotics, and genotyped using the Sequenom MassARRAY platform. Two hundred and thirty-six drug-naive patients treated with risperidone or quetiapine were analyzed independently. Additionally, we conducted pathway and expression analyses using several public bioinformatics databases.
resultsAfter correction for age and gender, the top 2 genome-wide significant SNPs with AIWG were located in the PTPRD gene (protein tyrosine phosphatase, receptor type D, 9p24-p23; rs10977144, P GWAS = 9.26E-09; rs10977154, P GWAS = 4.53E-08). The third most significant SNP was in the GFPT2 gene (glutamine-fructose-6-phosphate amidotransferase 2, 5q35.3; rs12386481, P GWAS = 1.98E-07). These results were validated in the replication cohort (rs10977144, P Replication = 4.30E-03; rs10977154, P Replication = 6.33E-03; rs12386481, P Replication =7.65E-03). These results were also verified in those patients initially exposed to risperidone and quetiapine (rs10977144, P = 1.97E-05; rs10977154, P = 2.04E-05; rs12386481, P = 1.97E-04). Pathway analyses showed that AIWG may involve in multiple pathways related to metabolic processes. Moreover, PTPRD mRNA might be highly expressed in brain regions, and the SNPs (rs10977144, rs1097154) also showed significant expression quantitative trait locus effects.
conclusionsOur findings indicate that PTPRD polymorphisms might modulate AIWG.
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