recently described how ApoE4 increases the burden of cerebral tau pathology, neuroinflammation, and brain atrophy in a P301S mouse model of frontotemporal dementia (FTD) and in vitro; they also demonstrated that in patients with a primary tauopathy, ApoE4 was associated with more severe regional neurodegeneration and that ApoE4+ AD patients with amyloid-β (Aβ) pathology showed faster disease progression [6]. This evidence concerns the gene APOE and frontotemporal dementia.