Therefore, it is important to understand the range of differences in LPL levels and function in human brain, particularly because LPL polymorphisms have been implicated in pathogenesis of stroke, Alzheimer’s disease, schizophrenia and other brain disorders (Myllykangas et al. 2001; Blain and Poirier 2004; Papassotiropoulos et al. 2005; Blain et al. 2006; Kostomarov et al. 2008; Wang C. et al. 2011; Xie et al. 2011; Munshi et al. 2012). This evidence concerns the gene LPL and early-onset autosomal dominant Alzheimer disease.