In contrast, we found elevated cortical Aβ deposition significantly predicted longitudinal cognitive decline regardless of APOE-ε4 status, which may be explained by that increased cortical Aβ burden may be related to other aspect of neurodegeneration [55] that resulting in cognitive decline in addition to hippocampal atrophy in APOE-ε4 non-carriers. This evidence concerns the gene APOE and hippocampal atrophy.