บทบาทของอะพอพโทซิสกับการเกิด blood-brain barrier breakdown ในมาลาเรียขึ้นสมอง

Abstract

          Malaria, a disease caused by protozoan parasites of the genus Plasmodium, is still a major problem in many parts of the world. Among the human malaria parasites, Plasmodium falciparum is the only species which sequesters in microvasculature and causes the most severe form of the disease, cerebral malaria. The mechanism underlying the onset of cerebral malaria is still not fully understood. Many research works have focussed attention on blood-brain barrier which is the key interface between the brain parenchyma and the parasite. Structurally and functionally studies of blood-brain barrier have provided some evidences for blood-brain barrier breakdown in cerebral malaria. However, the precise mechanism leading to the disruption of the blood-brain barrier seen in cerebral malaria is still unknown. It has been shown that sequestration, resulting from the interaction between parasite proteins on the surface of parasitized red blood cells and host endothelial cell adhesion molecules can cause activation of intracellular signalling pathways in endothelial cells including apoptosis which may be one of the mechanisms responsible for the blood-brain barrier breakdown in cerebral malaria. However, the fine mechanisms and signalling pathways implicating in this process remain to be further defined which, in turn, might lead to the new therapeutic intervention for the disease.