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Article: Genetic vulnerability to psychosis and cortical function: Epistatic effects between DAAO and G72

TitleGenetic vulnerability to psychosis and cortical function: Epistatic effects between DAAO and G72
Authors
KeywordsBipolar Disorder
Daao
Functional Magnetic Resonance Imaging
G72
Glutamate
Schizophrenia
Vulnerability
Issue Date2012
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htm
Citation
Current Pharmaceutical Design, 2012, v. 18 n. 4, p. 510-517 How to Cite?
AbstractRecent studies have described G72 and DAAO as susceptibility genes for schizophrenia and bipolar disorder. Both genes modulate glutamate neurotransmission, which plays a key role in neurocognitive function and is thought to be altered in these disorders. Moreover, in vitro transcription studies indicate that the two genes interact with each other at the molecular level. However, it is unclear how these genes affect cortical function and whether their effects interact with each other. The aim of this study was therefore to examine the impact of G72 rs746187 and DAAO rs2111902 genotypes on brain function in schizophrenia, bipolar disorder and healthy volunteers. We used functional magnetic resonance imaging and an overt verbal fluency paradigm to examine brain function in a total of 120 subjects comprising 40 patients with schizophrenia, 33 patients with bipolar I disorder and 47 healthy volunteers. A significant 3 way interaction between G72, DAAO and diagnosis was detected in the right middle temporal gyrus (x=60 y=-12 z=-12; z-score: 5.32; p<0.001 after family-wise error correction), accounting for 8.5% of the individual variance in activation. These data suggest that there is a nonadditive interaction between the effects of variations in the genes implicated in glutamate regulation that affects cortical function. Also, the nature of this interaction is different in patients and healthy controls, providing support for altered glutamate function in psychosis. Future studies could explore the effects of DAAO and G72 in individuals with prodromal symptoms of psychosis, in order to elucidate glutamate dysfunction in this critical phase of the disorder. © 2012 Bentham Science Publishers.
Persistent Identifierhttp://hdl.handle.net/10722/161255
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.586
References

 

DC FieldValueLanguage
dc.contributor.authorMechelli, Aen_US
dc.contributor.authorFusarPoli, Pen_US
dc.contributor.authorPrata, Den_US
dc.contributor.authorPapagni Sergio, Aen_US
dc.contributor.authorTognin, Sen_US
dc.contributor.authorKambeitz, Jen_US
dc.contributor.authorFu, Cen_US
dc.contributor.authorPicchioni, Men_US
dc.contributor.authorWalshe, Men_US
dc.contributor.authorToulopoulou, Ten_US
dc.contributor.authorBramon, Een_US
dc.contributor.authorMurray, Ren_US
dc.contributor.authorMcguire, Pen_US
dc.date.accessioned2012-08-23T06:11:29Z-
dc.date.available2012-08-23T06:11:29Z-
dc.date.issued2012en_US
dc.identifier.citationCurrent Pharmaceutical Design, 2012, v. 18 n. 4, p. 510-517en_US
dc.identifier.issn1381-6128en_US
dc.identifier.urihttp://hdl.handle.net/10722/161255-
dc.description.abstractRecent studies have described G72 and DAAO as susceptibility genes for schizophrenia and bipolar disorder. Both genes modulate glutamate neurotransmission, which plays a key role in neurocognitive function and is thought to be altered in these disorders. Moreover, in vitro transcription studies indicate that the two genes interact with each other at the molecular level. However, it is unclear how these genes affect cortical function and whether their effects interact with each other. The aim of this study was therefore to examine the impact of G72 rs746187 and DAAO rs2111902 genotypes on brain function in schizophrenia, bipolar disorder and healthy volunteers. We used functional magnetic resonance imaging and an overt verbal fluency paradigm to examine brain function in a total of 120 subjects comprising 40 patients with schizophrenia, 33 patients with bipolar I disorder and 47 healthy volunteers. A significant 3 way interaction between G72, DAAO and diagnosis was detected in the right middle temporal gyrus (x=60 y=-12 z=-12; z-score: 5.32; p<0.001 after family-wise error correction), accounting for 8.5% of the individual variance in activation. These data suggest that there is a nonadditive interaction between the effects of variations in the genes implicated in glutamate regulation that affects cortical function. Also, the nature of this interaction is different in patients and healthy controls, providing support for altered glutamate function in psychosis. Future studies could explore the effects of DAAO and G72 in individuals with prodromal symptoms of psychosis, in order to elucidate glutamate dysfunction in this critical phase of the disorder. © 2012 Bentham Science Publishers.en_US
dc.languageengen_US
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cpd/index.htmen_US
dc.relation.ispartofCurrent Pharmaceutical Designen_US
dc.subjectBipolar Disorderen_US
dc.subjectDaaoen_US
dc.subjectFunctional Magnetic Resonance Imagingen_US
dc.subjectG72en_US
dc.subjectGlutamateen_US
dc.subjectSchizophreniaen_US
dc.subjectVulnerabilityen_US
dc.titleGenetic vulnerability to psychosis and cortical function: Epistatic effects between DAAO and G72en_US
dc.typeArticleen_US
dc.identifier.emailToulopoulou, T:timothea@hku.hken_US
dc.identifier.authorityToulopoulou, T=rp01542en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.2174/138161212799316037en_US
dc.identifier.pmid22239582-
dc.identifier.scopuseid_2-s2.0-84856525206en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856525206&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issue4en_US
dc.identifier.spage510en_US
dc.identifier.epage517en_US
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridMechelli, A=6603693131en_US
dc.identifier.scopusauthoridFusarPoli, P=10044017500en_US
dc.identifier.scopusauthoridPrata, D=14632352500en_US
dc.identifier.scopusauthoridPapagni Sergio, A=55329584600en_US
dc.identifier.scopusauthoridTognin, S=26658653900en_US
dc.identifier.scopusauthoridKambeitz, J=36790051100en_US
dc.identifier.scopusauthoridFu, C=8502155300en_US
dc.identifier.scopusauthoridPicchioni, M=6507443795en_US
dc.identifier.scopusauthoridWalshe, M=8855469300en_US
dc.identifier.scopusauthoridToulopoulou, T=8855468700en_US
dc.identifier.scopusauthoridBramon, E=8089378900en_US
dc.identifier.scopusauthoridMurray, R=35406239400en_US
dc.identifier.scopusauthoridMcGuire, P=7101880438en_US
dc.identifier.issnl1381-6128-

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