Thus, the decline in the internalization of oAβ42 into BLECs is likely due to the properties of oAβ42, such as the size or structures of oligomers preventing its internalization into BLECs and their removal by the brain clearance system once Aβs are aggregated, which may explain Aβ oligomer-specific accumulation and toxicity in AD pathogenesis. The gene discussed is DDX41; the disease is Alzheimer disease.