Its loss in function greatly hinders the body's ability to mount an effective inflammatory response to infections, and explains why the ApoE−/− rodent model of human AD is prone to bacterial infections.4 Consequently, the ApoE−/− mouse model has become a critical research tool in investigating the relationship between periodontal infection and its contribution to the pathophysiology of systemic diseases7, , , –11; AD,8,11, , –14 cardiovascular disease and type II diabetes.15, –17. This evidence concerns the gene APOE and cardiovascular disorder.