Editorial Volume 15, Issue 5 pp 1232—1234

Figure 1. Proposed mechanism showing the parallels between age-associated brain and vascular amyloidosis, with both being mediated by sEVs and affected by cellular senescence. In the aorta, VSMC senescence acts as a trigger for medin accumulation, by increasing sEV secretion and enriching the ECM with HSPG2. These processes share similarities with the mechanisms regulating Aβ accumulation during AD and CAA, which could be key to understanding the build-up of medin in the brain and its colocalisation with other amyloid proteins. Created with https://BioRender.com.