SCARB1 and amyloidosis: Depleting SR‐B1 in J20 transgenic mice (overexpression of human Swedish KM670/671NL APP mutation) led to accelerated cerebrovascular and parenchymal amyloid plaque formation in the cortex and hippocampus, along with worsened neurocognitive deficits, suggesting a critical role of SR‐B1 and PVMs in Aβ clearance.17