Wilfried Rossoll

This study develops a scalable neuromuscular organoid platform to analyze drug responses in spinal muscular atrophy, showing distinct muscle and neuronal responses to SMN2 splicing modulators.

This study shows that TDP-43 aggregation in stress granules requires up-concentration and oxidative stress, leading to intra-condensate demixing and pathological aggregates.

This study identifies TDP-43-driven splicing dysregulation as a common mechanism in ALS, FTD, and Alzheimer's disease, linking them through mis-spliced mRNAs like APP.

The paper identifies context-dependent interactors of TDP-43 that regulate its dysfunction in ALS/FTLD using proximity labeling, mass spectrometry, and snRNA-seq integration.

This paper introduces ProPPr, a method for proteomic profiling of phospho-tau aggregates in tauopathies, revealing common and disease-specific proteins associated with these lesions.

This study shows that JNK activation by ER stress promotes SG assembly and neurodegeneration in C9orf72-mediated ALS/FTD through G3BP1 transcription.