ArticleNature communications2018
Variations in Dysbindin-1 are associated with cognitive response to antipsychotic drug treatment.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Dysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.International journal of molecular sciences · 2024Article
- Sex dimorphism controls dysbindin-related cognitive dysfunctions in mice and humans with the contribution of COMT.Molecular psychiatry · 2024Article
- Loss of dysbindin-1 in excitatory neurons in mice impacts NMDAR-dependent behaviors, neuronal morphology and synaptic transmission in the ventral hippocampus.Scientific reports · 2024Article
- Automation at the service of the study of executive functions in preclinical models.Scientific reports · 2023Article
- The Role of Dopamine D3 Receptors, Dysbindin, and Their Functional Interaction in the Expression of Key Genes for Neuroplasticity and Neuroinflammation in the Mouse Brain.International journal of molecular sciences · 2023Article
- Striatal dopaminergic alterations in individuals with copy number variants at the 22q11.2 genetic locus and their implications for psychosis risk: a [18F]-DOPA PET study.Molecular psychiatry · 2023Article
- Dopamine Dynamics and Neurobiology of Non-Response to Antipsychotics, Relevance for Treatment Resistant Schizophrenia: A Systematic Review and Critical Appraisal.Biomedicines · 2023Review
- Dysbindin-1A modulation of astrocytic dopamine and basal ganglia dependent behaviors relevant to schizophrenia.Molecular psychiatry · 2022Article
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
- The epistatic interaction between the dopamine D3 receptor and dysbindin-1 modulates higher-order cognitive functions in mice and humans.Molecular psychiatry · 2021Article
- Pharmacological and Genetic Evidence of Dopamine Receptor 3-Mediated Vasoconstriction in Isolated Mouse Aorta.Biomolecules · 2021Article
- Markers of copper transport in the cingulum bundle in schizophrenia.Schizophrenia research · 2021Article
- Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150Molecular brain · 2021Article
- Automatic Intra-/Extra-Dimensional Attentional Set-Shifting Task in Adolescent Mice.Frontiers in behavioral neuroscience · 2021Article
- Review
- Dopamine, Cognitive Impairments and Second-Generation Antipsychotics: From Mechanistic Advances to More Personalized Treatments.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Article
- The Discrete Paired-trial Variable-delay T-maze Task to Assess Working Memory in Mice.Bio-protocol · 2020Article
- Retinal biomarkers and pharmacological targets for Hermansky-Pudlak syndrome 7.Scientific reports · 2020Article
- Hermansky-Pudlak syndrome: Mutation update.Human mutation · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
22 authors at 10 institutions in 4 countries.
Funding
Abstract
Antipsychotics are the most widely used medications for the treatment of schizophrenia spectrum disorders. While such drugs generally ameliorate positive symptoms, clinical responses are highly variable in terms of negative symptoms and cognitive impairments. However, predictors of individual responses have been elusive. Here, we report a pharmacogenetic interaction related to a core cognitive dysfunction in patients with schizophrenia. We show that genetic variations reducing dysbindin-1 expression can identify individuals whose executive functions respond better to antipsychotic drugs, both in humans and in mice. Multilevel ex vivo and in vivo analyses in postmortem human brains and genetically modified mice demonstrate that such interaction between antipsychotics and dysbindin-1 is mediated by an imbalance between the short and long isoforms of dopamine D2 receptors, leading to enhanced presynaptic D2 function within the prefrontal cortex. These findings reveal one of the pharmacodynamic mechanisms underlying individual cognitive response to treatment in patients with schizophrenia, suggesting a potential approach for improving the use of antipsychotic drugs.
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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.