ArticleMammalian genome : official journal of the International Mammalian Genome Society2012
Genome-wide association mapping of loci for antipsychotic-induced extrapyramidal symptoms in mice.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Identifying key transcription factors for pharmacogenetic studies of antipsychotics induced extrapyramidal symptoms.Psychopharmacology · 2020Trial
- Gene expression changes following chronic antipsychotic exposure in single cells from mouse striatum.Molecular psychiatry · 2022Article
- Candidate Genes Encoding Dopamine Receptors as Predictors of the Risk of Antipsychotic-Induced Parkinsonism and Tardive Dyskinesia in Schizophrenic Patients.Biomedicines · 2021Review
- Article
- Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies.Frontiers in pharmacology · 2021Review
- Antipsychotic Behavioral Phenotypes in the Mouse Collaborative Cross Recombinant Inbred Inter-Crosses (RIX).G3 (Bethesda, Md.) · 2020Article
- Comparative genomic evidence for the involvement of schizophrenia risk genes in antipsychotic effects.Molecular psychiatry · 2018Article
- Revisiting Antipsychotic-induced Akathisia: Current Issues and Prospective Challenges.Current neuropharmacology · 2017Review
- Pharmacogenetic study of antipsychotic induced acute extrapyramidal symptoms in a first episode psychosis cohort: role of dopamine, serotonin and glutamate candidate genes.The pharmacogenomics journal · 2016Article
- Network analysis of gene expression in mice provides new evidence of involvement of the mTOR pathway in antipsychotic-induced extrapyramidal symptoms.The pharmacogenomics journal · 2016Article
- A Pharmacogenetic Discovery: Cystamine Protects Against Haloperidol-Induced Toxicity and Ischemic Brain Injury.Genetics · 2016Article
- Therapeutic Perspective on Tardive Syndrome with Special Reference to Deep Brain Stimulation.Frontiers in psychiatry · 2016Review
- The Founder Strains of the Collaborative Cross Express a Complex Combination of Advantageous and Deleterious Traits for Male Reproduction.G3 (Bethesda, Md.) · 2015Article
- Neurochemical Metabolomics Reveals Disruption to Sphingolipid Metabolism Following Chronic Haloperidol Administration.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015Article
- The role of Abcb5 alleles in susceptibility to haloperidol-induced toxicity in mice and humans.PLoS medicine · 2015Article
- Genetics of adverse reactions to haloperidol in a mouse diallel: a drug-placebo experiment and Bayesian causal analysis.Genetics · 2014Article
- Brain levels of the neurotoxic pyridinium metabolite HPP+ and extrapyramidal symptoms in haloperidol-treated mice.Neurotoxicology · 2013Article
- Testing two models describing how methylome-wide studies in blood are informative for psychiatric conditions.Epigenomics · 2013Article
- Effects of antipsychotics on dentate gyrus stem cell proliferation and survival in animal models: a critical update.Neural plasticity · 2012Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Tardive dyskinesia (TD) is a debilitating, unpredictable, and often irreversible side effect resulting from chronic treatment with typical antipsychotic agents such as haloperidol. TD is characterized by repetitive, involuntary, purposeless movements primarily of the orofacial region. In order to investigate genetic susceptibility to TD, we used a validated mouse model for a systems genetics analysis geared toward detecting genetic predictors of TD in human patients. Phenotypic data from 27 inbred strains chronically treated with haloperidol and phenotyped for vacuous chewing movements were subject to a comprehensive genomic analysis involving 426,493 SNPs, 4,047 CNVs, brain gene expression, along with gene network and bioinformatic analysis. Our results identified ~50 genes that we expect to have high prior probabilities for association with haloperidol-induced TD, most of which have never been tested for association with human TD. Among our top candidates were genes regulating the development of brain motor control regions (Zic4 and Nkx6-1), glutamate receptors (Grin1 and Grin2a), and an indirect target of haloperidol (Drd1a) that has not been studied as well as the direct target, Drd2.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.