This study demonstrates that EVs derived from amyloid-stressed neurons act as molecular messengers, mediating intercellular communication changes that influence both early and later stages of amyloid pathology, integrating in vitro data from amyloid-overexpressing N2A cells with in vivo data from APP/PSEN1 mouse brain cortices at different stages (6 and 9 months). The gene discussed is APP; the disease is amyloidosis.