This is a “truly significant advance” made by a team of researchers who have identified an important molecule involved in the development of cerebral malaria. The latter is one of the most deadly forms of malaria.
With experiments carried out on mice, the researchers came to the conclusion that the EphA2 protein is very important for the onset of the disease in the brain. By breaching this protein in mice, the researchers realized that it could be prevented, results that could suggest a functioning therapeutic strategy also for the version in humans.
Tracey Lamb is the study’s senior author and associate professor of pathology at the University of Utah Health. Cerebral malaria affects more than 575,000 people each year and is mainly present in sub-Saharan Africa, particularly three younger children. It causes fluids to escape from the brain into a coma. It kills 20% of infected people but survivors can develop serious symptoms that can last a lifetime such as seizures or mental health disorders.
One of the fundamental processes behind the development of cerebral malaria is the interruption of the blood-brain barrier, something that makes this disease deadly. It is a semipermeable cell wall that prevents the fluids of the brain’s nervous system from mixing with the bloodstream.
The researchers found that the EphA2 molecule breaks the blood-brain barrier causing the junctions between the cells to be less tight.