Cerebral malaria (CM) is a diffuse encephalopathy associated with coma and seizures commonly caused by Plasmodium falciparum (P. falciparum) in children with severe malaria.
Despite the breadth of models where GLP-1 is neuroprotective, ECM was not affected by liraglutide providing important insight into the pathogenesis of ECM.
The results indicate that the simultaneous evaluation of these bioactive molecules as quantifiable blood parameters may be helpful to get a better insight into the clinical syndromes in children with malaria.
The modern medical literature implicates malaria, and particularly the potentially fatal form of cerebral malaria, with a risk of neurocognitive impairment.
These findings indicate that inclusion of Cys in current formulations of ACT, or its use as adjunct therapy could improve the anti-plasmodial activity of artemisinin, decrease mortality in cerebral malaria patients, and prevent or delay the development and spread of artemisinin resistance.
This study clearly demonstrates the possibility of differentiating and identifying animals with CM at an early, pre-clinical stage.
Plasmodium falciparum infection causes a wide spectrum of diseases, including cerebral malaria, a potentially life-threatening encephalopathy.
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.
