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Investigations of apolipoprotein E ( APOE ) gene, the major genetic risk modifier for Alzheimer’s disease (AD), have yielded significant insights into the pathogenic mechanism. Among the three common coding variants,  APOE*ε4  increases, whereas  APOE*ε2  decreases the risk of late-onset AD compared with  APOE*ε3 . Despite increased understanding of the detrimental effect of  APOE*ε4 , it remains unclear how  APOE*ε2  confers protection against AD. Accumulating evidence suggests that  APOE*ε2  protects against AD through both amyloid-β (Aβ)-dependent and independent mechanisms. In addition,  APOE*ε2  has been identified as a longevity gene, suggesting a systemic effect of  APOE*ε2  on the aging process. However,  APOE*ε2  is not entirely benign;  APOE*ε2  carriers exhibit increased risk of certain cerebrovascular diseases and neurological disorders. Here, we review evidence from both human and animal studies demonstrating the protective effect of  APOE*ε2  against AD and propose a working model depicting potential underlying mechanisms. Finally, we discuss potential therapeutic strategies designed to leverage the protective effect of  APOE2  to treat AD.

APOE2: protective mechanism and therapeutic implications for Alzheimer’s disease