We found APOER2 Δex4-5, +ex6B, Δex18 isoform (unique to control) and APOER2 +ex6B, Δex14, Δex18 isoform (unique to AD) generated lower amounts of CTFs compared to APOER2-FL (45.4% and 59.4% decrease, p = 0.0017 and p < 0.0001 respectively) (Fig 6A and 6B), suggesting that APOER2 splice variants display differential cleavage events. This evidence concerns the gene LRP8 and Alzheimer disease.