Interestingly, despite the accumulating evidence that TG2 plays an important role in development and progression of Aβ pathology in both AD [39] and in the APP23 mouse model [26], in the current study absence of TG2 did not lead to significant differences in Aβ load and pathology, between APP23 and APP23/TG2−/− mice. This evidence concerns the gene TGM2 and Alzheimer disease.