To assess the causal relationship between disrupted mitochondrial fusion and AD-related deficits in the brain areas affected by AD, we utilized a genetic approach by crossing the Mfn2 conditional knockout mice (Mfn2loxP/loxP) with CaMKII-Cre mice, in which the Cre recombinase is expressed in the forebrain and result in specific ablation of Mfn2 in selective neurons in the hippocampus and cortex, brain areas that are heavily afflicted in AD. Here, CAMK2G is linked to Alzheimer disease.