PDGFRB and Cognitive impairment: Previous series in vitro and in vivo studies demonstrated that the extracellular domain of the PDGFRβ can be cleaved from cell membrane of brain pericytes in response to hypoxia or injurious stimuli,[18, 31] and the elevated levels of sPDGFRβ in CSF positively correlates with BBB disruption in patients with mild cognitive impairment.[16, 18] Intriguingly, we found that persistent PDGF‐BB treatment can induce its own receptor shedding, and increased sPDGFRβ was detected in the CM collected from PDGF‐BB‐treated pericytes.