Natalie M. Scherer

This study uses zebrafish models to show that human TDP-43 overexpression in motor neurons causes MND-like phenotypes through gain-of-function mechanisms, with distinct effects based on TDP-43 variant.

This study shows that SUMO modification affects TDP-43 phase separation and aggregation in zebrafish spinal neurons, linking post-translational changes to ALS pathology.

The paper validates and optimizes Bimolecular Fluorescence Complementation (BiFC) in zebrafish to study ALS-linked protein aggregate formation in vivo.