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Pathophysiology and neurologic sequelae of cerebral malaria

Journal

MALARIA JOURNAL
Volume 19, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12936-020-03336-z

Keywords

Cerebral malaria; Neurologic sequelae; Blood brain barrier; Inflammation; Heterogeneity

Funding

  1. NIH [RO3 NS087303-02, RO1 HL130649]
  2. Johns Hopkins Malaria Research Institute and Bloomberg Philanthropies

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Cerebral malaria (CM), results fromPlasmodium falciparuminfection, and has a high mortality rate. CM survivors can retain life-long post CM sequelae, including seizures and neurocognitive deficits profoundly affecting their quality of life. As thePlasmodiumparasite does not enter the brain, but resides inside erythrocytes and are confined to the lumen of the brain's vasculature, the neuropathogenesis leading to these neurologic sequelae is unclear and under-investigated. Interestingly, postmortem CM pathology differs in brain regions, such as the appearance of haemorragic punctae in whiteversusgray matter. Various host and parasite factors contribute to the risk of CM, including exposure at a young age, parasite- and host-related genetics, parasite sequestration and the extent of host inflammatory responses. Thus far, several proposed adjunctive treatments have not been successful in the treatment of CM but are highly needed. The region-specific CM neuro-pathogenesis leading to neurologic sequelae is intriguing, but not sufficiently addressed in research. More attention to this may lead to the development of effective adjunctive treatments to address CM neurologic sequelae.

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