Hardy and Selkoe (2002) suggest that one of the functions of ABCA7 in AD may be Aβ facilitated tauopathy: as Aβ deposition accumulates in cortical regions within the default mode network (DMN), it may lead to concurrent accumulation of tau tangles in the MTL via reciprocal connections through the entorhinal cortex (EC) (Pooler et al., 2015). This evidence concerns the gene ABCA7 and Alzheimer disease.