a1 Department of Psychosis Studies, Institute of Psychiatry, King's College London, King's Health Partners, UK
a2 St Andrew's Academic Centre, King's College London, Institute of Psychiatry, Northampton, UK
a3 Social, Genetic and Developmental Psychiatry, Institute of Psychiatry, King's College London, UK
a4 Department of Biostatistics, Institute of Psychiatry, King's College London, UK
Background Visual and verbal episodic memory deficits are putative endophenotypes for schizophrenia; however, the extent of any genetic overlap of these with schizophrenia is unclear. In this study, we set out to quantify the genetic and environmental contributions to variance in visual and verbal memory performance, and to quantify their genetic relationship with schizophrenia.
Method We applied bivariate genetic modelling to 280 twins in a classic twin study design, including monozygotic (MZ) and dizygotic (DZ) pairs concordant and discordant for schizophrenia, and healthy control twins. We assessed episodic memory using subtests of the Wechsler Memory Scale – Revised (WMS-R).
Results Genetic influences (i.e. heritability) contributed significantly to variance in immediate recall of both verbal memory and visual learning, and the delayed recall of verbal and visual memory. Liability to schizophrenia was associated with memory impairment, with evidence of significant phenotypic correlations between all episodic memory measures and schizophrenia. Genetic factors were the main source of the phenotypic correlations for immediate recall of visual learning material; both immediate and delayed recall of verbal memory; and delayed recall of visual memory that, for example, shared genetic variance with schizophrenia, which accounted for 88% of the phenotypic correlation (rph=0.41) between the two.
Conclusions Verbal memory and visual learning and memory are moderately heritable, share a genetic overlap with schizophrenia and are valid endophenotypes for the condition. The inclusion of these endophenotypes in genetic association studies may improve the power to detect susceptibility genes for schizophrenia.
(Received July 23 2009)
(Revised March 08 2010)
(Accepted April 03 2010)
(Online publication May 12 2010)
c1 Address for correspondence: Ms. S. F. Owens, Department of Psychosis Studies, Institute of Psychiatry, King's College London, King's Health Partners, De Crespigny Park, London SE5 8AF, UK. (Email: firstname.lastname@example.org)