One of the known mechanisms of cerebral malaria (CM) is the sequestration, within brain microvessels, of Plasmodium falciparum-parasitized red blood cells (PRBC), but also of leucocytes and platelets. Besides, CM is characterized by an overproduction of pro-inflammatory cytokines, inducing endothelial activation. This activation notably leads to the overexpression of adhesion molecules and to the release of microparticles, derived from various cell types within the vascular compartment. Microparticles are submicronic membranous elements carrying on their surface proteins from their cell of origin, which bestow on them specific biological properties. Because platelet-derived microparticles (PMP) represent the majority of circulating microparticles and because platelets have been shown to modulate PRBC cytoadherence, we analyzed the potential role of PMP in this cytoadherence.