“…The results of these studies have been inconsistent: some reported that Aβ auto-antibodies in AD were lower than in normal subjects [7, 8, 9, 10], some unaltered [11, 12, 13], and some increased [14, 15, 16]. The inconsistent results may have been caused by several factors including nonspecific bindings [17], serum Aβ interference [18], incorrect diagnosis [19, 20], structural conformation of Aβ1-42, and/or small sample size. Despite the relatively large number of studies being conducted, the epitope-specific binding and isotyping of the auto-antibodies against Aβ1-42 have not been reported.…”