Rapamycin, a drug recently approved for treating neurological diseases, was found to be effective in treating even cerebral malaria, research has found.
In another interesting twist, the researchers discovered that stopping food or reducing food intake during the first two days of infection could protect against the disease.
In animal model, treating mice with the drug rapamycin protected them against the neurological complications of cerebral malaria, they said revealing their new findings.
Since rapamycin is already approved for use in humans by US Food and Drug Administration, trials in humans for cerebral malaria treatment too with this drug is possible, said the researchers from Harvard T.H. Chan School of Public Health.
Cerebral malaria is a severe form of the disease and it may result in serious consequence of infection by the parasite Plasmodium falciparum, that is visible in the form of seizures, coma, and even death.
“The real importance of this work is the identification of unexpected molecular pathways underlying cerebral malaria that we can now target with existing drugs,” said senior author James Mitchell, who is an expert in genetics and complex diseases.
The researchers found that leptin – a hormone secreted from fat tissue with roles in suppressing appetite, but also in activating adaptive immune and inflammatory responses – is increased upon infection in a mouse model of cerebral malaria.
This hormone also turns out to be a major bad actor in promoting neurological symptoms and death due to cerebral malaria.
Reducing leptin using a variety of means, either genetically, pharmacologically, or nutritionally by reducing food intake during the first two days of infection, protected against cerebral malaria, the findings showed.
The researchers also found that leptin acted primarily on cytotoxic T cells by turning on the well-studied mTOR protein, for which pharmacologic inhibitors are readily available.
The study has been published in the journal Nature Communications.