Cerebral malaria (CM) is one of the most serious complications of Plasmodium falciparum infection. It is characterized by sequestration of parasitized red blood cells (PRBC) in cerebral capillaries and venules. Although the exact cause of CM remains unclear, current evidence has clearly implicated metabolic disturbances and host immune responses. Studies on mouse CM models suggest the involvement of host cells and in particular platelets. These results led us to study the role of platelets in human CM. Our findings demonstrated that significantly greater accumulation of platelets occurred in capillaries and venules of Malawian patients who died from CM than from other diseases. We also assessed the role of platelets in cytoadherence of PRBCs using PRBC adhering only on CD36, platelets and endothelial cells (EC) constitutively devoid of CD36. Cultures using the three components showed that platelets played a role in inducing cytoadherence of PRBC on EC via a cellular bridging resistant to physiological flow conditions. Having established the link between platelets and sequestration, the next step will be to examine the link between platelets and CM. A combination of approaches from different disciplines will be needed to gain further insight into the mechanisms underlying the complications of malaria.