Skip to main content
Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Therapeutic approaches targeting Apolipoprotein E function in Alzheimer’s disease

Fig. 1

Congruence 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 list

Back to article page