Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology?

Research output: Contribution to journalReviewResearchpeer-review

  1. Brain Changes Induced by Electroconvulsive Therapy Are Broadly Distributed

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. A phenome-wide association and Mendelian Randomisation study of polygenic risk for depression in UK Biobank

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. The Duffy-null genotype and risk of infection

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Association between Mental Disorders and Subsequent Medical Conditions

    Research output: Contribution to journalJournal articleResearchpeer-review

  5. Genome-wide gene-environment analyses of major depressive disorder and reported lifetime traumatic experiences in UK Biobank

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

The diagnosis of schizophrenia rests on clinical criteria that cannot be assessed in animal models. Together with absence of a clear underlying pathology and understanding of what causes schizophrenia, this has hindered development of informative animal models. However, recent large-scale genomic studies have identified copy number variants (CNVs) that confer high risk of schizophrenia and have opened a new avenue for generation of relevant animal models. Eight recurrent CNVs have reproducibly been shown to increase the risk of schizophrenia by severalfold: 22q11.2(del), 15q13.3(del), 1q21(del), 1q21(dup), NRXN1(del), 3q29(del), 7q11.23(dup), and 16p11.2(dup). Five of these CNVs have been modeled in animals, mainly mice, but also rats, flies, and zebrafish, and have been shown to recapitulate behavioral and electrophysiological aspects of schizophrenia. Here, we provide an overview of the schizophrenia-related phenotypes found in animal models of schizophrenia high-risk CNVs. We also discuss strengths and limitations of the CNV models, and how they can advance our biological understanding of mechanisms that can lead to schizophrenia and can be used to develop new and better treatments for schizophrenia.

Original languageEnglish
JournalBiological Psychiatry
Volume85
Issue number1
Pages (from-to)13-24
Number of pages12
ISSN0006-3223
DOIs
Publication statusPublished - 1 Jan 2019

    Research areas

  • CNV, Copy number variant, Genetic animal model, Genetics, Schizophrenia, Schizophrenia-related phenotype, Dopamine, Rats, Positron-Emission Tomography, Neural Cell Adhesion Molecules, DNA Copy Number Variations, Animals, Models, Animal, Mice, Psychotic Disorders

ID: 55270354