Cerebral malaria may predispose children to mental health disorders, possibly as a consequence of ischaemic neural injury.
Cerebral malaria is caused by Plasmodium falciparum. Atorvastatin (AVA) is a pentasubstituted pyrrole, which has been tested as an adjuvant in the treatment of cerebral malaria.
Cerebral malaria is a well-known complication of Plasmodium falciparum malaria.
Most patients with cerebral malaria (CM) sustain cerebral microvascular sequestration of Plasmodium falciparum-infected red blood cells (iRBCs).
Severe malaria is a density-dependent disease that comprises infected-erythrocyte sequestration, with or without monocytic infiltration, as seen in renal, placental, and lung tissues from severe malaria patients.
Taken together, paediatric CM brain volume was associated with products of the PLA 2 pathway and inflammatory cytokines.
There is significant evidence that brain-infiltrating CD8+ T cells play a central role in the development of experimental cerebral malaria (ECM) during Plasmodium berghei ANKA infection of C57BL/6 mice
A paper published twenty years ago should have attracted more attention (NM Anstey et al., J Exp Med 1996, 184, 557-567) : the suppression of NO synthesis in cerebral malaria appears to enhance pathogenesis and increased NO synthesis protects against clinical disease. The work was based on in vivo results obtained in Tanzanian children. Already five years earlier the killing of Plasmodium falciparum in vitro by nitric oxide derivatives (NO, nitrite, nitrate) had been demonstrated (KA Rockett et al., Infection and Immunity, 1991, 59, 3280-3283).
Cerebral malaria (CM) is a major contributor to malaria deaths, but its pathophysiology is not well understood.
Aside from antimalarials, there is currently no treatment for cerebral malaria, a fulminant neurological complication of P. falciparum infection that is a leading cause of death in African children.
