Preeclampsia (PE) is a pregnancy-specific condition characterized by high blood pressure and signs of organ damage. While it primarily affects the cardiovascular and renal systems, PE is also associated with neurological complications often attributed to hypertension-induced alterations in cerebral blood vessels. Small extracellular vesicles (sEVs) have recently emerged as potential drivers of blood-brain barrier (BBB) disruption by impacting its cellular components. We investigated whether circulating sEVs in plasma, including those derived from the placenta, contribute to cerebrovascular alterations in PE.  The impact of sEVs on the function of brain endothelial cells (BECs), microglia, and astrocytes was studied, focusing on potential effects related to BBB disruption. Circulating sEVs were isolated from plasma samples of healthy and PE pregnancies and tested in human-based mono-, bi-, or tri-culture models using transwell and microfluidic (BBB-on-a-chip) systems. Our results revealed that PE-sEVs disrupted endothelial barrier integrity evidenced by increased permeability and decreased expression of tight-junction proteins. Furthermore, PE-sEV crossed the BEC layer in a bi-culture transwell setup and reached microglia. There, PE-sEVs were phagocytosed and transferred their miRNA cargo, inducing upregulation of Iba1 expression and amoeboid morphology, suggesting microglial activation. Similarly, using BBB-on-a-chip and direct stimulation models, PE-sEVs triggered a reactive astrocyte phenotype, characterized by increased GFAP expression, elevated secretion of the pro-inflammatory cytokine IL-6, and enhanced migratory capacity. The activation of astrocytes and microglia may amplify neuroinflammation in PE, potentially contributing to exacerbated BBB dysfunction. Our findings suggest that sEVs could play a crucial role in the placenta-brain axis in PE, leading to maternal brain injury by transmitting signals of placental damage. Understanding this mechanism could offer valuable insights for both diagnostic and therapeutic strategies in managing the neurological complications of PE.