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

Research output: Contribution to journal › Review › Research › peer-review

Standard

Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology? / Forsingdal, Annika; Jørgensen, Trine Nygaard; Olsen, Line; Werge, Thomas; Didriksen, Michael; Nielsen, Jacob.

In: Biological Psychiatry, Vol. 85, No. 1, 2019, p. 13-24.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Forsingdal, A, Jørgensen, TN, Olsen, L, Werge, T, Didriksen, M & Nielsen, J 2019, 'Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology?', Biological Psychiatry, vol. 85, no. 1, pp. 13-24. https://doi.org/10.1016/j.biopsych.2018.07.004

APA

Forsingdal, A., Jørgensen, T. N., Olsen, L., Werge, T., Didriksen, M., & Nielsen, J. (2019). Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology? Biological Psychiatry, 85(1), 13-24. https://doi.org/10.1016/j.biopsych.2018.07.004

Vancouver

Forsingdal A, Jørgensen TN, Olsen L, Werge T, Didriksen M, Nielsen J. Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology? Biological Psychiatry. 2019;85(1):13-24. https://doi.org/10.1016/j.biopsych.2018.07.004

Author

Forsingdal, Annika ; Jørgensen, Trine Nygaard ; Olsen, Line ; Werge, Thomas ; Didriksen, Michael ; Nielsen, Jacob. / Can Animal Models of Copy Number Variants That Predispose to Schizophrenia Elucidate Underlying Biology?. In: Biological Psychiatry. 2019 ; Vol. 85, No. 1. pp. 13-24.

Bibtex

@article{4ea41c7abce14789b82d69da98239c40,
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 = "Animals, DNA Copy Number Variations, Dopamine, Mice, Models, Animal, Neural Cell Adhesion Molecules, Positron-Emission Tomography, Psychotic Disorders, Rats, Schizophrenia",
author = "Annika Forsingdal and J{\o}rgensen, {Trine Nygaard} and Line Olsen and Thomas Werge and Michael Didriksen and Jacob Nielsen",
year = "2019",
doi = "10.1016/j.biopsych.2018.07.004",
language = "English",
volume = "85",
pages = "13--24",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier",
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

PY - 2019

Y1 - 2019

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 - Animals

KW - DNA Copy Number Variations

KW - Dopamine

KW - Mice

KW - Models, Animal

KW - Neural Cell Adhesion Molecules

KW - Positron-Emission Tomography

KW - Psychotic Disorders

KW - Rats

KW - Schizophrenia

U2 - 10.1016/j.biopsych.2018.07.004

DO - 10.1016/j.biopsych.2018.07.004

M3 - Review

C2 - 30144930

VL - 85

SP - 13

EP - 24

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 1

ER -

ID: 226869049