Fig. 1From: Therapeutic approaches targeting Apolipoprotein E function in Alzheimer’s diseaseCongruence of the effects of apoE between human studies, mouse models of AD and in vitro cell culture models. apoE influences multiple pathways in the AD cascade in an isoform-dependent manner. We compared the concurrence of available research data in mouse models and in vitro models versus clinical studies with human patients. Pathways indicated in the green color indicate a broad consensus of APOE isoform effect between mice, men and in vitro models where E4 is associated with an increased pathological risk when compared to E3 or E2 isoforms (E4>E3>E2). Data from the pathways indicated in yellow background are not in complete congruence between human studies, mouse model experiments and in vitro data. Interestingly, even within a set of studies in a given experimental system, there is disagreement in between the observations, which is marked by superscripted symbols that refers to the disparate studies. The symbols (< or >) indicate the order of increased pathological effect for the APOE isoforms. The effects listed here are specific to only classical AD pathology and excludes data on α-synuclein and TDP43 which are associated with diseases such as PDD and DLB. *, conflicting reports [see ref 40]; #, conflicting reports [see ref 41]; ¶, studies compared APOE4 TR, Apoe KO, and wild type C57BL6J mice. The references presented are representative and not an exhaustive listBack to article page