File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Selective attention deficits reflect increased genetic vulnerability to schizophrenia
  • Basic View
  • Metadata View
  • XML View
TitleSelective attention deficits reflect increased genetic vulnerability to schizophrenia
 
AuthorsFilbey, FM1
Toulopoulou, T1
Morris, RG1
McDonald, C1
Bramon, E1
Walshe, M1
Murray, RM1
 
KeywordsAttention
Biological markers
Familial
Obligate carriers
Schizophrenia
 
Issue Date2008
 
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/schres
 
CitationSchizophrenia Research, 2008, v. 101 n. 1-3, p. 169-175 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.schres.2008.01.019
 
AbstractBackground: Impairment in attention is prominent in schizophrenia and may be a valuable genetic indicator for vulnerability to this disease. Aims: We set out to characterize the attention deficits that may be associated with genetic liability to schizophrenia. Methods: We compared attention performance in 55 people with schizophrenia, 95 of their first-degree relatives, and 61 unrelated controls. We also segregated presumed obligate carriers of genetic risk (POCs, N = 12) and compared their performance with that of controls. Results: Although the relatives of people with schizophrenia did not significantly differ from the normal controls on the tasks of attention, their scores were significantly ordered such that patients > relatives > normal controls during tasks of sustained and selective attention as measured by the Jonckheere-Terpstra Test (p < .05). Additionally, POCs were significantly worse than normal controls during selective attention tasks such as the Stroop (p = .03) and Letter Cancellation Task (p = .04). Conclusions: Heterogeneity in the first-degree relatives may have diluted the attention deficits present in those who are at genetic risk for schizophrenia. On the other hand, our findings in the more homogeneous group of POCs suggest that selective attention may be an indicator of genetic liability for schizophrenia. © 2008 Elsevier B.V. All rights reserved.
 
ISSN0920-9964
2013 Impact Factor: 4.426
2013 SCImago Journal Rankings: 3.163
 
DOIhttp://dx.doi.org/10.1016/j.schres.2008.01.019
 
ISI Accession Number IDWOS:000256212200019
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorFilbey, FM
 
dc.contributor.authorToulopoulou, T
 
dc.contributor.authorMorris, RG
 
dc.contributor.authorMcDonald, C
 
dc.contributor.authorBramon, E
 
dc.contributor.authorWalshe, M
 
dc.contributor.authorMurray, RM
 
dc.date.accessioned2011-09-27T03:03:13Z
 
dc.date.available2011-09-27T03:03:13Z
 
dc.date.issued2008
 
dc.description.abstractBackground: Impairment in attention is prominent in schizophrenia and may be a valuable genetic indicator for vulnerability to this disease. Aims: We set out to characterize the attention deficits that may be associated with genetic liability to schizophrenia. Methods: We compared attention performance in 55 people with schizophrenia, 95 of their first-degree relatives, and 61 unrelated controls. We also segregated presumed obligate carriers of genetic risk (POCs, N = 12) and compared their performance with that of controls. Results: Although the relatives of people with schizophrenia did not significantly differ from the normal controls on the tasks of attention, their scores were significantly ordered such that patients > relatives > normal controls during tasks of sustained and selective attention as measured by the Jonckheere-Terpstra Test (p < .05). Additionally, POCs were significantly worse than normal controls during selective attention tasks such as the Stroop (p = .03) and Letter Cancellation Task (p = .04). Conclusions: Heterogeneity in the first-degree relatives may have diluted the attention deficits present in those who are at genetic risk for schizophrenia. On the other hand, our findings in the more homogeneous group of POCs suggest that selective attention may be an indicator of genetic liability for schizophrenia. © 2008 Elsevier B.V. All rights reserved.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationSchizophrenia Research, 2008, v. 101 n. 1-3, p. 169-175 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.schres.2008.01.019
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.schres.2008.01.019
 
dc.identifier.epage175
 
dc.identifier.isiWOS:000256212200019
 
dc.identifier.issn0920-9964
2013 Impact Factor: 4.426
2013 SCImago Journal Rankings: 3.163
 
dc.identifier.issue1-3
 
dc.identifier.pmid18291626
 
dc.identifier.scopuseid_2-s2.0-42749097977
 
dc.identifier.spage169
 
dc.identifier.urihttp://hdl.handle.net/10722/141849
 
dc.identifier.volume101
 
dc.languageeng
 
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/schres
 
dc.publisher.placeNetherlands
 
dc.relation.ispartofSchizophrenia Research
 
dc.relation.referencesReferences in Scopus
 
dc.subjectAttention
 
dc.subjectBiological markers
 
dc.subjectFamilial
 
dc.subjectObligate carriers
 
dc.subjectSchizophrenia
 
dc.titleSelective attention deficits reflect increased genetic vulnerability to schizophrenia
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Filbey, FM</contributor.author>
<contributor.author>Toulopoulou, T</contributor.author>
<contributor.author>Morris, RG</contributor.author>
<contributor.author>McDonald, C</contributor.author>
<contributor.author>Bramon, E</contributor.author>
<contributor.author>Walshe, M</contributor.author>
<contributor.author>Murray, RM</contributor.author>
<date.accessioned>2011-09-27T03:03:13Z</date.accessioned>
<date.available>2011-09-27T03:03:13Z</date.available>
<date.issued>2008</date.issued>
<identifier.citation>Schizophrenia Research, 2008, v. 101 n. 1-3, p. 169-175</identifier.citation>
<identifier.issn>0920-9964</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/141849</identifier.uri>
<description.abstract>Background: Impairment in attention is prominent in schizophrenia and may be a valuable genetic indicator for vulnerability to this disease. Aims: We set out to characterize the attention deficits that may be associated with genetic liability to schizophrenia. Methods: We compared attention performance in 55 people with schizophrenia, 95 of their first-degree relatives, and 61 unrelated controls. We also segregated presumed obligate carriers of genetic risk (POCs, N = 12) and compared their performance with that of controls. Results: Although the relatives of people with schizophrenia did not significantly differ from the normal controls on the tasks of attention, their scores were significantly ordered such that patients &gt; relatives &gt; normal controls during tasks of sustained and selective attention as measured by the Jonckheere-Terpstra Test (p &lt; .05). Additionally, POCs were significantly worse than normal controls during selective attention tasks such as the Stroop (p = .03) and Letter Cancellation Task (p = .04). Conclusions: Heterogeneity in the first-degree relatives may have diluted the attention deficits present in those who are at genetic risk for schizophrenia. On the other hand, our findings in the more homogeneous group of POCs suggest that selective attention may be an indicator of genetic liability for schizophrenia. &#169; 2008 Elsevier B.V. All rights reserved.</description.abstract>
<language>eng</language>
<publisher>Elsevier BV. The Journal&apos;s web site is located at http://www.elsevier.com/locate/schres</publisher>
<relation.ispartof>Schizophrenia Research</relation.ispartof>
<subject>Attention</subject>
<subject>Biological markers</subject>
<subject>Familial</subject>
<subject>Obligate carriers</subject>
<subject>Schizophrenia</subject>
<title>Selective attention deficits reflect increased genetic vulnerability to schizophrenia</title>
<type>Article</type>
<description.nature>link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/j.schres.2008.01.019</identifier.doi>
<identifier.pmid>18291626</identifier.pmid>
<identifier.scopus>eid_2-s2.0-42749097977</identifier.scopus>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-42749097977&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>101</identifier.volume>
<identifier.issue>1-3</identifier.issue>
<identifier.spage>169</identifier.spage>
<identifier.epage>175</identifier.epage>
<identifier.isi>WOS:000256212200019</identifier.isi>
<publisher.place>Netherlands</publisher.place>
</item>
Author Affiliations
  1. King's College London