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

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@article{25920f4b04354928a959b659a3c9d2d6,
title = "Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology?",
abstract = "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.",
keywords = "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",
author = "Annika Forsingdal and J{\o}rgensen, {Trine Nygaard} and Line Olsen and Thomas Werge and Michael Didriksen and Jacob Nielsen",
note = "Copyright {\circledC} 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.",
year = "2019",
month = "1",
day = "1",
doi = "10.1016/j.biopsych.2018.07.004",
language = "English",
volume = "85",
pages = "13--24",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier Inc",
number = "1",

}

RIS

TY - JOUR

T1 - Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology?

AU - Forsingdal, Annika

AU - Jørgensen, Trine Nygaard

AU - Olsen, Line

AU - Werge, Thomas

AU - Didriksen, Michael

AU - Nielsen, Jacob

N1 - Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - CNV

KW - Copy number variant

KW - Genetic animal model

KW - Genetics

KW - Schizophrenia

KW - Schizophrenia-related phenotype

KW - Dopamine

KW - Rats

KW - Positron-Emission Tomography

KW - Neural Cell Adhesion Molecules

KW - DNA Copy Number Variations

KW - Animals

KW - Models, Animal

KW - Mice

KW - Psychotic Disorders

UR - http://www.scopus.com/inward/record.url?scp=85051924988&partnerID=8YFLogxK

U2 - 10.1016/j.biopsych.2018.07.004

DO - 10.1016/j.biopsych.2018.07.004

M3 - Review

VL - 85

SP - 13

EP - 24

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 1

ER -

ID: 55270354