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Schizophrenia Bulletin Advance Access published online on June 17, 2008
Schizophrenia Bulletin, doi:10.1093/schbul/sbn064
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Catechol-O-Methyltransferase Val158Met Polymorphism and Antisaccade Eye Movements in Schizophrenia

Haraldur Magnus Haraldsson1,2, Ulrich Ettinger3, Brynja B. Magnusdottir2,3, Thordur Sigmundsson2, Engilbert Sigurdsson2, Andres Ingason4 and Hannes Petursson2
2 Division of Psychiatry, Landspitali University Hospital, Hringbraut, 101 Reykjavik, Iceland
3 Institute of Psychiatry, King's College London, London, UK
4 Research Institute of Biological Psychiatry, Copenhagen University Hospital, Roskilde, Denmark

1 To whom correspondence should be addressed; tel: +354 543 4067, fax: +354 543 4816, e-mail: hmagnus{at}landspitali.is.

The catechol-O-methyltransferase (COMT) enzyme catabolizes dopamine. The val158met single nucleotide polymorphism (rs4680) in the COMT gene has received considerable attention as a candidate gene for schizophrenia as well as for frontally mediated cognitive functions. Antisaccade performance is a good measure of frontal lobe integrity. Deficits on the task are considered a trait marker for schizophrenia. The aim of this study was to investigate the association of COMT val158met polymorphism with antisaccade eye movements in schizophrenia patients and healthy controls. Schizophrenia patients (N = 105) and healthy controls (N = 95) underwent infrared oculographic assessment of antisaccades. Subjects were genotyped for COMT val158met and divided into 3 groups according to genotype (val/val, val/met, and met/met). Patients displayed significantly more reflexive errors, longer and more variable latency, and lower amplitude gain than controls (all P < 0.02). A greater number of val158 alleles was associated with shorter (P = 0.045) and less variable (P = 0.028) antisaccade latency and, nonsignificantly, with lower reflexive error rate (P = 0.056). None of these variables showed a group-by-genotype interaction (P > 0.1). There were no significant associations of genotype with measures of amplitude gain or spatial error (P > 0.2). The results suggest that COMT val158 carrier status is associated with better performance on the antisaccade task. Possible explanations of this finding are discussed.

Keywords: COMT val158met polymorphism / dopamine / oculomotor / antisaccade / schizophrenia / endophenotype


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