Dr. Mensa-Wilmot studies African trypanosomiasis, more commonly known as African sleeping sickness.

Dr. Mensa-Wilmot earned his Ph.D. from the Department of Biological Chemistry at Johns Hopkins University. He has been at the University of Georgia since the early 1990s.

Trypanosomiasis is caused by infection by the single-celled trypanosome parasite. It is transmitted by the tsetse fly, and gets into the human bloodstream after an insect bite. Infection has two phases — the first is characterized by fever and headaches, while the parasite multiplies within the host. During the second phase, the parasite crosses the blood-brain barrier and infects the central nervous system. In this phase, sleep is highly disturbed, there can be Parkinson’s-like trembling, and in some cases, psychiatric symptoms. Left untreated, trypanosomiasis is fatal, and damage done during the second phase is irreversible. It has been reported across sub-Saharan Africa and close to 70 million people are considered at “high risk”.

Current drugs for trypanosomiasis are toxic and hard to administer, leaving ample room for improvement. Dr. Mensa-Wilmot’s research focuses on screening drug candidates, and a recent paper focused on one such candidate: AEE788. This compound was shown previously to interact with three different signaling proteins in the trypanosome, and Dr. Mensa-Wilmot’s goal was to better understand why this compound was toxic to the parasite. They found that AEE788 blocked the trypanosomes from duplicating themselves, specifically by inhibiting DNA replication.

They suggest that this effect makes AEE788 good for future research on trypanosomes for two reasons. First, it suggests that the three proteins AEE788 interferes with are important for initiation of DNA replication - previous research had found that what we know about how DNA replication initiation works in most species isn’t applicable to trypanosomes. So this gives us some new directions to look into.

Second, we now have a method for synchronizing parasite cells in the cell cycle: researchers can add the drug for a few hours, blocking each cell from beginning replication once it reaches that point, and then later wash all the drug away — releasing all of those cells to replicate at the same time. This makes it easier to see how replication works in this species and how consistent it is across cells.