Tauopathies are neurodegenerative diseases marked by the misfolding and aggregation of the tau protein, leading to synaptic dysfunction and neuronal loss. Melissa Borgen’s lab is using C. elegans models to map the genetic and molecular pathways that drive these processes.
Her team discovered a new prodegenerative role of RPM-1/Phr1/MycBP2 in tau-mediated neuronal damage. This NIH-funded research has identified three downstream pathways influencing degeneration, with key contributions from graduate students Xinxing Ding, Aidan Anderson and Evan Landreth. Their findings promise to shed light on the early mechanisms of neurodegeneration and open new avenues for therapeutic intervention.
Pictured Above:
Top: Diagram of worm motor cord; green denotes GABAergic motor neurons
Bottom: Representative images of each genotype. Wild-type worms have fully intact motor cords, shown by GFP coverage along the length of the animal. Rpm-1 mutant motor cords are also intact. The tauopathy model (TauV337M) induces “breaks” in the GFP (white arrowheads), indicating degeneration of axons or neurons in the motor cord. When rpm-1 is knocked out in the Tau model, there are fewer breaks.
