Marco Morsch

This study identifies SFPQ as a contributor to TDP-43 pathology through a bidirectional feedback loop, showing SFPQ dysregulation drives TDP-43 mislocalization and aggregation.

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 uses upconversion nanoparticles and real-time imaging to visualize vascular permeability changes in zebrafish, revealing distinct transcellular and paracellular transport mechanisms and demonstrating enhanced BBB penetration with functionalized nanoparticles.

This study shows that animals can be engineered to express microbial enzymes to convert methylmercury into volatile mercury, reducing its toxicity and accumulation.

This study identifies a transient protein folding response in early TDP-43 disease that reduces aggregation, with DNAJB5 as a protective factor, and shows proteomic similarities between mouse and human TDP-43 proteinopathies.

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

This study shows riluzole does not improve disease outcomes in a mouse model of ALS with cytoplasmic TDP-43 pathology.

This study examines SFPQ dysregulation in ALS patients, finding increased intron retention, reduced mRNA expression in motor cortex, and cytoplasmic aggregates.

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

The paper identifies cyclin F interactors using BioID and shows that ALS/FTD-associated cyclin F mutations disrupt paraspeckle protein homeostasis, particularly RBM14 levels in patient tissue.