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dc.contributor.authorROBERTSON, IANen
dc.contributor.authorGILL, MICHAELen
dc.contributor.authorMORRIS, DEREKen
dc.contributor.authorGARAVAN, HUGHen
dc.contributor.authorCORVIN, AIDENen
dc.contributor.authorFOXE, JOHNen
dc.date.accessioned2010-09-16T10:02:16Z
dc.date.available2010-09-16T10:02:16Z
dc.date.issued2008en
dc.date.submitted2008en
dc.identifier.citationDonohoe G, Morris D.W., De Sanctis P, Magno E, Montesi J, Garavan H, Robertson I, Javitt D, Gill M, Corvin A, Fox J., Early Visual Processing Deficits in Dysbindin-Associated Schizophrenia, Biological Psychiatry, 63, 5, 2008, 484 - 489en
dc.identifier.otherYen
dc.identifier.urihttp://hdl.handle.net/2262/40654
dc.descriptionPUBLISHEDen
dc.descriptionPMID: 17945199en
dc.description.abstractBackground: Variation at the dysbindin gene (DTNBP1) has been associated with increased risk for schizophrenia in numerous independent samples and recently with deficits in general and domain-specific cognitive processing. The relationship between dysbindin risk variants and sensory-level deficits in schizophrenia remains to be explored. We investigated P1 performance, a component of early visual processing on which both patients and their relatives show deficits, in carriers and noncarriers of a known dysbindin risk haplotype. Methods: Event-related potential responses to simple visual isolated-check stimuli were measured using high-density electrical scalp recordings in 26 individuals meeting DSM-IV criteria for schizophrenia, comprising 14 patients who were carriers of the dysbindin risk haplotype and 12 patients who were nonrisk haplotype carriers. Results: Carriers of the dysbindin risk haplotype demonstrated significantly reduced P1 amplitudes compared with noncarriers. A large effect size of d = .89 was calculated for the difference in P1 amplitude over scalp sites where the deficit was maximal. Conclusions: The P1 deficits associated with a dysbindin risk haplotype previously identified in our sample presents functional confirmation of its deleterious effect on brain activity. Building on evidence of dysbindin?s role in higher cognitive function, these early visual processing deficits suggest a generalized role for dysbindin in brain function and is likely to be part of the mechanism by which illness susceptibility is mediated.en
dc.format.extent484en
dc.format.extent489en
dc.language.isoenen
dc.relation.ispartofseriesBiological Psychiatryen
dc.relation.ispartofseries63en
dc.relation.ispartofseries5en
dc.rightsYen
dc.subjectPsychiatryen
dc.subjectschizophreniaen
dc.titleEarly Visual Processing Deficits in Dysbindin-Associated Schizophreniaen
dc.typeJournal Articleen
dc.contributor.sponsorScience Foundation Ireland (SFI)en
dc.type.supercollectionscholarly_publicationsen
dc.type.supercollectionrefereed_publicationsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/mgillen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/morrisdwen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/irobertsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/acorvinen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/garavanhen
dc.identifier.rssinternalid46230en
dc.subject.TCDThemeGenes & Societyen
dc.subject.TCDThemeNeuroscienceen
dc.identifier.rssurihttp://dx.doi.org/10.1016/j.biopsych.2007.07.022en


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