Interestingly, OBSCs from an alternative amyloidosis mouse model (5xFAD) showed similar changes, with a significant increase in PECAM-1+ vessel length and area (Supplementary Fig. 2a–c) and a substantial increase in filopodia number (Supplementary Fig. 2d, e) compared to WT littermate controls, indicative of conserved mechanisms between models. The gene discussed is PECAM1; the disease is amyloidosis.