Cerebral Malaria

Malfunction of the fibrocytes type 1 in the spiral ligament and disruption of the blood labyrinth barrier, resulting in a breakdown of the endocochlear potential, are major causes for hearing impairment in murine cerebral malaria.

In 2010 there were a number of publications discussing the relevance of rodent models for the study of human cerebral malaria (HCM).

A Th1 response is required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM).

The 371G allele of RNASE3 is associated with susceptibility to CM and forms part of a risk associated haplotype GGA defined by the markers: rs2073342 (G-allele), rs2233860 (G-allele) and rs8019343 (A-allele) respectively.

This research describes the use of novel antimalarial combinations of the new artemisinin derivative artemiside, a 10-alkylamino artemisinin.

These results suggest that at the time of admission plasma levels of ANG-2 and ratio of ANG-2/ANG-1 are clinically informative biomarkers to predict fatal CM from MM cases while they have limited usefulness to discriminate fatal CM outcomes in a pool of CM cases in endemic settings of Central India.

We review here what is currently known regarding biomarkers for CM outcomes. A Pub Med literature search was performed using the following search terms: "malaria," "cerebral malaria," "biomarkers," "mortality" and "neurological sequelae."

Cerebral malaria is a severe form of the disease that may result, in part, from an overt inflammatory response during infection by Plasmodium falciparum.

The genetic association observed in the present study implies that the regulation of platelet-decorated ULVWF strings by ADAMTS13 may play a role in the development of cerebral malaria.

Using these settings, reinvasion of normal mouse erythrocytes by the parasite was obtained in vitro over two weeks with preservation of the infectivity in vivo.