In ApoD-null-APP-PS1 mice, models of amyloidogenic AD without ApoD expression, loss of ApoD increases the amyloid plaque load by almost two-fold, while overexpression of human ApoD (HApoD-APP-PS1 mice) decreases by 60% the amyloid-β 1-40 peptides and decreases by 34% the insoluble amyloid-β 1-42 [100]. Here, APP is linked to Alzheimer disease.