Skip to main content Accessibility help
×
Home
Hostname: page-component-544b6db54f-rlmms Total loading time: 0.187 Render date: 2021-10-19T12:35:04.418Z Has data issue: true Feature Flags: { "shouldUseShareProductTool": true, "shouldUseHypothesis": true, "isUnsiloEnabled": true, "metricsAbstractViews": false, "figures": true, "newCiteModal": false, "newCitedByModal": true, "newEcommerce": true, "newUsageEvents": true }

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
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

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.

Type
Open Peer Commentary
Copyright
Copyright © Cambridge University Press 2008

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Arguello, P. A. & Gogos, J. A. (2006) Modeling madness in mice: One piece at a time. Neuron 52(1):179–96.CrossRefGoogle ScholarPubMed
Brown, A. S. (2006) Prenatal infection as a risk factor for schizophrenia. Schizophrenia Bulletin 32(2):200202.CrossRefGoogle Scholar
Crawley, J. N. (2007) Mouse behavioral assays relevant to the symptoms of autism. Brain Pathology 17(4):448–59.CrossRefGoogle ScholarPubMed
Crow, J. F. (2000) The origins, patterns and implications of human spontaneous mutation. Nature Reviews. Genetics 1(1):4047.CrossRefGoogle ScholarPubMed
El-Saadi, O., Pedersen, C. B., McNeil, T. F., Saha, S., Welham, J., O'Callaghan, E., Cantor-Graae, E., Chant, D., Mortensen, P. B. & McGrath, J. (2004) Paternal and maternal age as risk factors for psychosis: Findings from Denmark, Sweden and Australia. Schizophrenia Research 67 (2–3):227–36.CrossRefGoogle ScholarPubMed
Emanuel, B. S. & Saitta, S. C. (2007) From microscopes to microarrays: Dissecting recurrent chromosomal rearrangements. Nature Reviews. Genetics 8(11):869–83.CrossRefGoogle ScholarPubMed
Eyles, D., Brown, J., Mackay-Sim, A., McGrath, J. & Feron, F. (2003) Vitamin D3 and brain development. Neuroscience 118(3):641–53.CrossRefGoogle ScholarPubMed
Fatemi, S. H., Cuadra, A. E., El Fakahany, E. E., Sidwell, R. W. & Thuras, P. (2000) Prenatal viral infection causes alterations in nNOS expression in developing mouse brains. Neuroreport 11(7):1493–96.CrossRefGoogle ScholarPubMed
Fatemi, S. H., Reutiman, T. J., Folsom, T. D. & Sidwell, R. W. (2007) The role of cerebellar genes in pathology of autism and schizophrenia. Cerebellum 116. Online article, available at: http://dx.doi.org/10.1080/14734220701392969.CrossRefGoogle Scholar
Hornig, M., Weissenbock, H., Horscroft, N. & Lipkin, W. I. (1999) An infection-based model of neurodevelopmental damage. Proceedings of the National Academy of Sciences USA 96(21):12102–107.CrossRefGoogle ScholarPubMed
Keller, M. C. & Miller, G. (2006) Resolving the paradox of common, harmful, heritable mental disorders: Which evolutionary genetic models work best? Behavioral and Brain Sciences 29(4):385452.CrossRefGoogle ScholarPubMed
Kesby, J. P., Burne, T. H., McGrath, J. J. & Eyles, D. W. (2006) Developmental vitamin D deficiency alters MK 801-induced hyperlocomotion in the adult rat: An animal model of schizophrenia. Biological Psychiatry 60(6):591–96.CrossRefGoogle Scholar
Lee, J. A. & Lupski, J. R. (2006) Genomic rearrangements and gene copy-number alterations as a cause of nervous system disorders. Neuron 52(1):103–21.CrossRefGoogle ScholarPubMed
Libbey, J. E., Sweeten, T. L., McMahon, W. M. & Fujinami, R. S. (2005) Autistic disorder and viral infections. Journal of Neurovirology 11(1):110.CrossRefGoogle ScholarPubMed
Lipska, B. K., Swerdlow, N. R., Geyer, M. A., Jaskiw, G. E., Braff, D. L. & Weinberger, D. R. (1995) Neonatal excitotoxic hippocampal damage in rats causes post-pubertal changes in prepulse inhibition of startle and its disruption by apomorphine. Psychopharmacology (Berlin) 122(1):3543.CrossRefGoogle ScholarPubMed
Lupski, J. R. (2007) Genomic rearrangements and sporadic disease. Nature Genetics 39 (Suppl. 7):S4347.CrossRefGoogle ScholarPubMed
Malaspina, D., Harlap, S., Fennig, S., Heiman, D., Nahon, D., Feldman, D. & Susser, E. S. (2001) Advancing paternal age and the risk of schizophrenia. Archives of General Psychiatry 58(4):361–67.CrossRefGoogle ScholarPubMed
McGrath, J., Feron, F., Burne, T. H. J., Mackay-Sim, A. & Eyles, D. (2003) The neurodevelopmental hypothesis of schizophrenia: A review of recent developments. Annals of Medicine 35(2):8693.CrossRefGoogle ScholarPubMed
Meyer, U., Feldon, J., Schedlowski, M. & Yee, B. K. (2006a) Immunological stress at the maternal-foetal interface: A link between neurodevelopment and adult psychopathology. Brain, Behavior, and Immunity 20(4):378–88.CrossRefGoogle ScholarPubMed
Meyer, U., Nyffeler, M., Engler, A., Urwyler, A., Schedlowski, M., Knuesel, I., Yee, B. K. & Feldon, J. (2006b) The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. Journal of Neuroscience 26(18):4752–62.CrossRefGoogle ScholarPubMed
Moy, S. S., Nadler, J. J., Young, N. B., Perez, A., Holloway, L. P., Barbaro, R. P., Wilson, L. M., Threadgill, D. W., Lauder, J. M., Magnuson, T. R. & Crawley, J. M. (2007) Mouse behavioral tasks relevant to autism: Phenotypes of 10 inbred strains. Behavioral Brain Research 176(1):420.CrossRefGoogle ScholarPubMed
Nithianantharajah, J. & Hannan, A. J. (2007) Dynamic mutations as digital genetic modulators of brain development, function and dysfunction. Bioessays 29(6):525–35.CrossRefGoogle ScholarPubMed
Pearson, C. E., Nichol Edamura, K. & Cleary, J. D. (2005) Repeat instability: Mechanisms of dynamic mutations. Nature Reviews. Genetics 6(10):729–42.CrossRefGoogle ScholarPubMed
Perrin, M. C., Brown, A. S. & Malaspina, D. (2007) Aberrant epigenetic regulation could explain the relationship of paternal age to schizophrenia. Schizophrenia Bulletin 33(6):1270–73.CrossRefGoogle Scholar
Reichenberg, A., Gross, R., Weiser, M., Bresnahan, M., Silverman, J., Harlap, S., Rabinowitz, J., Shulman, C., Malaspina, D., Lubin, G., Knobler, H. Y., Davidson, M. & Susser, E. (2006) Advancing paternal age and autism. Archives of General Psychiatry 63(9):1026–32.CrossRefGoogle ScholarPubMed
Sebat, J., Lakshmi, B., Malhotra, D., Troge, J., Lese-Martin, C., Walsh, T., Yamrom, B., Yoon, S., Krasnitz, A., Kendall, J., Leotta, A., Pai, D., Zhang, R., Lee, Y. H., Hicks, J., Spence, S. J., Lee, A. T., Puura, K., Lehtimäki, T., Ledbetter, D., Gregersen, P. K., Bregman, J., Sutcliffe, J. S., Jobanputra, V., Chung, W., Warburton, D., King, M. C., Skuse, D., Geschwind, D. H., Gilliam, T. C., Ye, K. & Wigler, M. (2007) Strong association of de novo copy number mutations with autism. Science 316(5823):445–49.CrossRefGoogle ScholarPubMed
Sipos, A., Rasmussen, F., Harrison, G., Tynelius, P., Lewis, G., Leon, D. A. & Gunnell, D. (2004) Paternal age and schizophrenia: A population based cohort study. British Medical Journal 329(7474):1070.CrossRefGoogle ScholarPubMed
Vorstman, J. A. S., Morcus, M. E. J., Duijff, S. N., Klaassen, P. W. J., Heineman-de Boer, J. A., Beemer, F. A., Swaab, H., Kahn, R. S. & van Engeland, H. (2006) The 22q11.2 deletion in children: High rate of autistic disorders and early onset of psychotic symptoms. Journal of the American Academy of Child and Adolescent Psychiatry 45(9):1104–13.CrossRefGoogle ScholarPubMed

Send article to Kindle

To send this article to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle. Find out more about sending to your Kindle.

Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

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

Send article to Dropbox

To send this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Dropbox.

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

Send article to Google Drive

To send this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Google Drive.

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

Reply to: Submit a response

Please enter your response.

Your details

Please enter a valid email address.

Conflicting interests

Do you have any conflicting interests? *