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This paper discusses generally the potential effects of genetic markers on individual differences in cognitive performance. Research on the role of two genetic markers related to the immune system—complement factor C3 and haptoglobin—and one genetic marker—apolipoprotein E (ApoE)—and the interaction with environmental conditions of cognitive support at memory encoding and retrieval are discussed in particular. Data from an ongoing longitudinal study are used to illustrate that the two markers of the immune system are strongly associated with performance in episodic memory tasks, although there is no association to semantic memory. Cross-sectional data reveal a relatively weak association between apolipoprotein E and memory performance. Preliminary analyses of longitudinal data reveal a somewhat stronger association between this genetic marker and some aspects of episodic memory performance.

This study of the general population examined interactions of the gene Apolipoprotein E (APOE) and/or lipid levels, and their effects on cognitive change. A MANCOVA model based on longitudinal data (with a 5 year follow-up) obtained from the Betula study (n = 1777; age 35–85 years) was used. The significant two-way and three-way interaction effects detected were equally frequent in tests of episodic and semantic memory. A difference in the distribution of interaction effects on episodic and semantic memory decline was also found. Men demonstrated the worst cognitive development as shown by significant two-way interaction effects on episodic memory whereas two-way interaction effects among women resulted in the worst semantic memory development. This result is discussed from the viewpoint that tests of episodic and semantic memory have different cognitive demands.This study focuses on how interaction effects of the gene APOE and vascular risk factors (such as lipid levels) affect cognitive abilities and also whether the interaction effects vary across age and sex. In this study, the main focus is on interaction effects as a phenomenon in itself.

Acknowledgements We would like to thank all of the patients, relatives and control individuals who participated in the study. We are indebted to the late Prof. Walter Muir, Chair of Developmental Psychiatry and Honorary Consultant in Learning Disability Psychiatry, University of Edinburgh, who initiated these studies and whose work was dedicated to the welfare of the patients who generously participated. We are also grateful to Mrs. Pat Malloy for her assistance with DNA collection and MAQ assays screening of the Scottish samples. The Scottish sample collection was supported by a grant from the Chief Scientist Office (CSO), part of the Scottish Government Health and Social Care Directorates. This research was funded by grants from the CSO to B.S.P. (grant CZB/4/610), The Academy of Medical Sciences/Wellcome Trust to M.J. (grant R41455) and The RS Macdonald Charitable Trust (grant D21419 together with J.H.), the Swedish Research Council (grants 2003-5158 and 2006-4472), the Medical Faculty, Umeå University, and the County Councils of Västerbotten and Norrbotten, Sweden, as well as by grants from the Fund for Scientific Research Flanders (FWO-F), the Industrial Research Fund (IWT) and the Special Research Fund of the University of Antwerp, Belgium. M.J. is funded by a Wellcome Trust Clinical Research Fellowship for MB PhD graduates (R42811). We acknowledge the contribution of the personnel of the VIB Genetic Service Facility (http://www.vibgeneticservicefacility.be/) for the genetic analysis of the Swedish samples. Research nurses Gunnel Johansson, Lotta Kronberg, Tage Johansson and Lisbeth Bertilsson are thankfully acknowledged for their help and expertise. The Betula Study was funded by the Swedish Research Council (grants 345-2003-3883 and 315-2004-6977). We also acknowledge the contribution by the staff in the Betula project ; Peer reviewed ; Publisher PDF