A study in preclinical Alzheimer’s research reported that microglial CD31 hinders amyloid-beta clearance and worsens pathology in a 5×FAD mouse model. The work identified CD31 as a critical suppressor of Aβ removal, implicating a specific receptor-driven mechanism behind disease progression. The findings, framed as a mechanism shift, point to microglial targeting strategies beyond the traditional focus on dopamine loss or purely neuronal pathways, with potential relevance for therapeutic selection in Alzheimer’s disease.