Sleeping sickness refers to a range of different parasitic diseases. The one subject to the recent study is African trypanosomiasis. This is caused by a single-celled animal (protozoa) called Trypanosoma brucei. The disease is spread by the tsetse fly. The symptoms begin with fevers, headaches, itchiness, and joint pains. After this, confusion, poor coordination, numbness and trouble sleeping follows. The latter symptom gives the disease its name. The pattern of the disease is in cycles of epidemics, hitting different communities in waves. Rural populations are at the greatest risk.
Currently, the only medication that can treat all forms of the disease is Melarsoprol. However, the chemical carries a risk of toxicity. The parasite has a developed resistance against other treatments.
The research breakthrough is based on a defense mechanism that the protozoan organism uses to resist drug treatments. The parasite is able to produce an enzyme that can cut through the active ingredient in chemical treatments, rendering the chemical ineffective. A newly developed chemical side steps this and actually tricks the parasite into taking a material that resembles a nutrient.
Researchers have discovered, Pharmaceutical Processing reports, that the parasite requires nutrients absorbed from the blood, called purines, to survive. It is this dependency that a new candidate treatment seeks to target. The concept is to use an analogous material that the parasite will absorb but instead of providing nutrients acts to instead kill the parasite.
In tests the trial material has been used to successfully cure mice of the disease. Given this success, the next phase is to test the material on primates, with human trials the ultimate goal.
The study has been conducted at Umeå University in Sweden. The findings are published in the Journal of Biological Chemistry. The research is titled “Trypanosoma brucei methylthioadenosine phosphorylase protects the parasite from the antitrypanosomal effect of deoxyadenosine: implications for the pharmacology of adenosine antimetabolites.”
