Hannah Fleckenstein

This study develops an iPSC-based model with enhanced endothelial identity to study malaria parasite interactions and pathogenesis in vitro.

The paper investigates how innate immune responses to Plasmodium falciparum contribute to blood-brain barrier disruption in cerebral malaria using an in vitro model.

This paper shows that Plasmodium falciparum impairs Ang-1 secretion by pericytes in a 3D brain microvessel model, leading to vascular dysfunction that can be partially reversed with Ang-1 or AKB-9778.

This study shows that Plasmodium falciparum egress products disrupt BBB endothelial junctions and activate JAK-STAT signaling, leading to increased permeability and suggesting therapeutic targets.