Impact of Inflammatory Cytokine Profiles on Neurological Complications in Pediatric Cerebral Malaria:
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Date
2025
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Research Output Journal of Engineering and Scientific Research
Abstract
Pediatric cerebral malaria (CM), a severe neurological manifestation of Plasmodium falciparum infection, disproportionately affects children under five in sub-Saharan Africa and remains a leading cause of mortality and long-term neurological morbidity despite effective antiparasitic treatment. Neurological sequelae such as cognitive impairment, motor dysfunction, and behavioral disorders result primarily from immunopathological processes, with inflammatory cytokines emerging as key mediators. This conceptual review explored the pivotal role of inflammatory cytokine profiles, including TNF-α, IL-1β, IL-6, and IFN-γ, in the pathogenesis of cerebral injury in pediatric CM. These cytokines contribute to blood-brain barrier disruption, endothelial activation, neuroinflammation, and excitotoxicity, all of which exacerbate cerebral dysfunction in the developing brain. Furthermore, the immature pediatric immune system, marked by an exaggerated pro-inflammatory response and insufficient regulatory mechanisms, amplifies vulnerability to cytokine-mediated damage. The article was developed using a narrative synthesis methodology, drawing on interdisciplinary literature from immunopathology, neurobiology, and pediatric infectious disease. Potential interventions targeting cytokine signaling pathways, including anti-TNF therapies, cytokine receptor antagonists, and neuroprotective agents, are discussed as future directions to mitigate neurological injury. Ultimately, understanding the immunological underpinnings of pediatric CM is essential for designing adjunctive therapies that preserve neurological function and improve long-term outcomes in affected children