The aims of the present study were: i) to enlarge our previous GWAS sample in order to increase the power to detect new susceptibility genes by raising them above the threshold of genome-wide significance, and ii) to test, for the first time, for the presence of a polygenic component to the development of AD. A polygenic component is defined as the presence of a multitude of small genetic effects (with individual effect sizes below the threshold for detection at the level of single markers within a GWAS), being measured as a summed effect. The latter method has recently been applied successfully to test for a polygenic contribution to schizophrenia and bipolar disorder (Purcell, Wray, Stone et al. 2009). For a detailed explanation of this approach see Purcell et al. (2009). In simple terms, the polygenic score approach uses information concerning association findings for several ten thousand SNPs from a discovery sample to calculate a summary score for each individual in a target sample. Subsequent analyses are performed to test whether the cases in the target sample have different scores to
