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The development of malaria-induced neurocognitive and behavioral sequelae is not entirely understood. We hypothesize that liver dysfunction caused by Plasmodium infection is responsible for malaria-induced neurocognitive and behavioral sequelae. Our metabolic hypothesis not only explains neurocognitive sequelae after cerebral malaria (CM) but also after other severe, non-severe, and asymptomatic malaria infections.
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Martins et al. (2024) studied this question.
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