the top genes nearest the strongest variants from the LOAD GWAS may not be actual disease genes. These loci require further investigations to account for this possibility. Additionally, our criteria for selection of the top cisSNPs, requiring significance in both ADs and non–ADs, might be too stringent, thereby leading to some false negative results. Finally, it may be possible to identify additional disease-related expression variants by focusing on those that have differential influence in disease vs. non-disease tissue, although this was not a focus of analysis in this study. Given that our non–AD tissue also consisted of subjects with other neurodegenerative diseases, there may be more similarities with the AD tissue, making it more difficult to detect variants with differential disease-related expression-associations in our current study. Nevertheless, we did find associations with cisSNPs for ABCA7, a novel AD risk locus gene [28], [47] and MAPT [52], [53], [24], [54] implicated in AD.
