Therefore, we sought to examine immunohistochemically the effect of Artemether therapy on expression of amyloid-β (Figures 9(a) and 9(d)) and tau hyperphosphorylation (Figures 9(a)–9(c)) pathology in the brain cortex of 3xTg-AD mice using β-amyloid, phospho-tau (ser 416, which has been demonstrated to be a major phosphorylation site of CaMK II in Alzheimer's disease brain) and pan-tau (T-tau) antibodies. Here, CAMK2G is linked to early-onset autosomal dominant Alzheimer disease.