“…Its occurrence is when activated platelets during the course of malaria infection [38] release microparticles that modulate the sequestration of parasitized erythrocytes (PRBC) on the brain endothelium, platelets aggregate [39][40][41]. Mechanism of platelets induced CM is, assumed that through contact dependent pro-apoptotic effect of platelets on TNF-α activated human brain micro-vascular endothelial cells (HBEC) [42].…”