APOE4 knock-in mice and AD patients exhibited substantial lipid droplet accumulation in ChP [33], where high expression levels of lipid transporting associated proteins (e.g., Apoe, Clu and Lrp1) implied that lipid dysregulation in the brain parenchyma of AD patients may be attributed to impaired lipid-processing specialization of this compartment. This evidence concerns the gene LRP1 and Alzheimer disease.