These findings suggest that clusterin and APOE may work cooperatively in this mouse model to reduce amyloid deposition and illustrate the complexity of understanding Aβ-clusterin interactions in vivo. A more recent study in APP/PS1 mice showed that CLU-KO shifts deposition of Aβ from plaques to accumulation in the cerebrovasculature, resulting in increased amyloid angiopathy but, surprisingly, reduced hemorrhage and inflammation (Wojtas et al., 2017). This evidence concerns the gene CLU and amyloidosis.