This study aimed at testing the extent to which IVIG (Gammagard) alters expression of NFT tau epitopes with the CA1 pyramidal neurons of the 3xTg AD mouse model. In addition to evaluating the effects of IVIG therapy on NFT pathology, the authors also compared gene expression profiles of plasma isolated from placebo and IVIG-treated 3xTg mice to identify putative mechanistic markers for the pathogenic events underlying both disease progression and therapeutic modification  by IVIG. The results show that IVIG abrogates the age dependent hippocampal tau pathological burden observed in the 3xTg mouse model of AD. Moreover, the gene expression profiling experiments revealed that IVIG may slow tangle propagation by stabilizing or increasing cytoskeletal and calcium signaling plasticity and phosphorylation-based cellular homeostatic mechanisms in the face of mounting AD pathology in these mice. The data presented suggest that IVIG is a useful tool for understanding the mechanisms of NFT formation and prevention that will aid in the further design of IVIG clinical trials for the treatment of AD.