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. Infections, Anti-infective Agents, and Risk of Deliberate Self-harm and Suicide in a Young Cohort: A Nationwide Study

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Volume of the Human Hippocampus and Clinical Response Following Electroconvulsive Therapy

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Autism spectrum disorder and attention deficit hyperactivity disorder have a similar burden of rare protein-truncating variants

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Clinical association to FKBP5 rs1360780 in patients with depression

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. A large-scale genomic investigation of susceptibility to infection and its association with mental disorders in the Danish population

    Research output: Contribution to journalJournal articleResearchpeer-review

  5. Genetic risk scores for major psychiatric disorders and the risk of postpartum psychiatric disorders

    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
ISSN0006-3223
DOIs
Publication statusPublished - 1 Jan 2019

ID: 55270354