In Alzheimer’s disease, Aβ pathology progresses in a spatiotemporal pattern through the connected brain structures, involving the accumulation of neurotoxic Aβ in the blood vessels and brain parenchyma.6,12 At the BBB, LRP1 acts as a main transporter for Aβ.11,14,15,17 It is thus safe to assume that decline in the expression of LRP1, reported with normal ageing and Alzheimer’s disease,24–26 results in a deficient Aβ clearance across the BBB. The gene discussed is LRP1; the disease is early-onset autosomal dominant Alzheimer disease.