no specified criteria. Since these classification criteria differ, certain subjects would be eligible for inclusion as “affected” in some studies but not in others. Less stringent diagnostic criteria could differentiate the patient and control groups to a smaller extent, potentially altering observed effect sizes for ALDH2 504lys. Second, studies using mixed-sex samples may yield different results than studies using only male or female subjects, especially if the sexes are mixed in only patient or control group. Third, in terms of recruitment strategy, the allele differences between patients and controls may be greater in the samples recruited from clinical treatment than in the samples from general population due to well-recognized ascertainment bias. Fourth, the genetic effects of ALDH2 504lys on AD may change longitudinally over the course of illness. Fifth, the samples were not in Hardy-Weinberg equilibrium (HWE) (Zintzaras 2008) in several studies. Of the control samples that were not in HWE, either the samples were small or the disequilibrium was not highly significant. Disequilibrium in patients supports that the gene may be related to AD because the genotype distributions observed differ from those expected by chance; however, disequilibrium in controls is more likely to reflect genotyping error and thus distort
