Studies on genetic or population isolates offer a powerful approach to identifying genetic variants accounting for disease heritability due to their relatively reduced genetic, environmental and phenotypic variability. The Old Order Amish of Lancaster County represent a genetic isolate of European ancestry where a number of disease causing genetic mutations have been identified including several Mendelian disorders [6,7]. We have recently reported an in-depth genetic analysis of a large, multigenerational Amish pedigree with BPD [8]. Although the small sample size may have hindered the identification of risk variants or a common etiologic pathway, a set of credible candidate genes were identified for further examination in other Amish pedigrees or in large-scale population-based studies. In addition to genetic studies, gene expression studies on postmortem brain tissue from BPD patients and controls have been conducted as an orthogonal approach to elucidate mechanisms underlying BPD [9–15]. A major caveat of post mortem brain studies, however, is the difficulty in differentiating disease etiology-associated changes (e.g. gene expression) from those caused by post-mortem artifact, life-long illness or prior drug treatment. Recent advances in human induced
