Authors: Liu M, Wilson NO, Cespedes J, Ford B, Botchway F, Gyasi R, Adjei AA, Stiles JK
Cerebral malaria (CM) is the most severe neurological complication of infection with Plasmodium falciparum. Over 575,000 cases are reported annually and children in sub-Saharan Africa are the most affected. A subset of survivors develops neurological, behavioral and cognitive deficits. Cerebral malaria is characterized by the sequestration of Plasmodium falciparum-infected erythrocytes (pRBC), increased circulating free heme, inflammation, brain swelling, vascular dysfunction and brain tissue injury.
The pathogenesis of CM associated neuro-cognitive sequelae is poorly understood: coma develops through multiple mechanisms and several mechanisms may mediate the accompanying brain injury – how an intravascular parasite causes brain injury remains misunderstood. Understanding the injury and repair processes in infected hosts is important to develop appropriate neuro-protective interventions. Recent studies have identified NRG-1, an 8 kDa secreted cytoprotective trophic factor, encoded by the neuregulin/NRG-1 gene located on the short arm of chromosome 8 [4], which mediates injury/repair mechanisms in stroke [1], cardiovascular diseases [2] and tumors [3] in addition to attenuating experimental cerebral malaria (ECM) in a murine model.
