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Apolipoprotein E ( APOE ) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer’s disease mainly by modulating amyloid-β pathology.  APOE  ε4 is also shown to exacerbate neurodegeneration and neuroinflammation in a tau transgenic mouse model. To further evaluate the association of  APOE  genotype with the presence and severity of tau pathology, we express human tau via an adeno-associated virus gene delivery approach in human  APOE  targeted replacement mice. We find increased hyperphosphorylated tau species, tau aggregates, and behavioral abnormalities in mice expressing  APOE  ε2/ε2. We also show that in humans, the  APOE  ε2 allele is associated with increased tau pathology in the brains of progressive supranuclear palsy (PSP) cases. Finally, we identify an association between the  APOE  ε2/ε2 genotype and risk of tauopathies using two series of pathologically-confirmed cases of PSP and corticobasal degeneration. Our data together suggest  APOE  ε2 status may influence the risk and progression of tauopathy.

APOE ε2 is associated with increased tau pathology in primary tauopathy