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Animal models may help fractionate shared and discrete pathways underpinning schizophrenia and autism

Published online by Cambridge University Press:  26 June 2008

Thomas H. J. Burne ,
Darryl W. Eyles  and
John J. McGrath
Thomas H. J. Burne
Affiliation:
Queensland Centre for Mental Health Research, The Queensland Brain Institute, The University of Queensland, St Lucia, Brisbane, 4072, Australia. t.burne@uq.edu.auhttp://www.qbi.uq.edu.aueyles@uq.edu.auhttp://www.qbi.uq.edu.aujohn_mcgrath@qcmhr.uq.edu.auhttp://www.qbi.uq.edu.au
Darryl W. Eyles
Affiliation:
Queensland Centre for Mental Health Research, The Queensland Brain Institute, The University of Queensland, St Lucia, Brisbane, 4072, Australia. t.burne@uq.edu.auhttp://www.qbi.uq.edu.aueyles@uq.edu.auhttp://www.qbi.uq.edu.aujohn_mcgrath@qcmhr.uq.edu.auhttp://www.qbi.uq.edu.au
John J. McGrath
Affiliation:
Queensland Centre for Mental Health Research, The Queensland Brain Institute, The University of Queensland, St Lucia, Brisbane, 4072, Australia. t.burne@uq.edu.auhttp://www.qbi.uq.edu.aueyles@uq.edu.auhttp://www.qbi.uq.edu.aujohn_mcgrath@qcmhr.uq.edu.auhttp://www.qbi.uq.edu.au
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Abstract

Crespi & Badcock (C&B) present an appealing and parsimonious synthesis arguing that schizophrenia and autism are differentially regulated by maternal versus paternal genomic imprinting, respectively. We argue that animal models related to schizophrenia and autism provide a useful platform to explore the mechanisms outlined by C&B. We also note that schizophrenia and autism share certain risk factors such as advanced paternal age. Apart from genomic imprinting, copy number variants related to advanced paternal age may also contribute to the differential trajectory of brain development associated with autism and schizophrenia.

Information

Type
Open Peer Commentary
Information
Behavioral and Brain Sciences , Volume 31 , Issue 3 , June 2008 , pp. 264 - 265
Copyright
Copyright © Cambridge University Press 2008

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