In order to determine whether the degree of interaction between the worm and GWAS genes was greater, or less, than one would expect by chance we systematically compared the overlap between the worm and GWAS +1 interactomes for each of the worm-screen genes. One possible explanation for the highly interconnected nature of the worm screen hits could be summarised as “sociological bias”. In this context, we hypothesise that previous worm screens have yielded similar gene lists and that the consequent interest in the field has PF-4217903 956905-27-4 resulted in more interaction data being deposited in the BioGrid database. In support of this hypothesis, we find that the screens for Ab and polyQ yield 27 common genes, and we find that 20 of them are highly interconnected genes. Even if there is such a sociological bias, this does not invalidate subsequent conclusion because we have carefully compensated for differences in network connectivity. Another explanation is that genetic modifiers of worm phenotypes really do have more highly interconnected protein products as compared to the average gene. Highly interconnected gene products are likely involved in more biological pathways than less connected ones; so it may be that highly interconnected gene products are more likely to influence disease-related processes as assessed by a genetic screen. However this cannot explain why there is no similar interconnectivity bias when the same analysis is applied to the GWAS white+grey zone genes. Indeed, the distribution of connectivity of the products of white+grey zone genes is remarkably similar to that of the general population of genes. This is likely to be explained by the presence of many false-positive genes in this list. Three of these genes have +1 interactome overlaps with GWAS white+grey zone genes that are smaller than one would expect by chance, suggesting that they are artifactual modifiers of the worm phenotype. Consequently, these data should dissuade us from investigating the ribosomal and proteasomal functions of these genes in AD. By contrast, the remaining 4 genes exhibited a greater than expected +1 interactome overlap with the GWAS white+grey zone genes. Furthermore, we found that two of these genes are both members of the TRiC/CCT chaperone that has a number of substrates including actin and tubulin. This chaperone complex was also enriched in the gene ontology analysis of the worm hits. CCT8 and MOB4 have not been observed as modifiers in any other worm models of neurodegeneration however TCP1 and ACTB RNAi also modify polyQ toxicity.