Two of the three haplotypes showed significant inverse associations with ND, suggesting protective functions against the development of ND. Given (a) APBB1 is important in the etiology of AD and PD, (b) tobacco smoking is inversely associated with AD and PD, and (c) APBB1 variants are associated with ND, this study provides further evidence regarding the potential connection between smoking and both AD and PD at the gene level. In addition, a protective effect of a deletion in intron 13 of APBB1 for late-onset AD has been reported (Cousin et al. 2003; Hu et al. 2002; Lambert et al. 2000) although other studies failed to replicate such an association (Guenette et al. 2000; Prince et al. 2001). Despite these discrepancies observed among different studies, it is still suggested that APBB1 remains a potential candidate for a genetic study with AD (Cousin et al. 2003).
