The Intersection of TMEM106B Fibrils, TDP-43 Pathology & Lysosomal Function in Neurodegeneration
- How TMEM106B genetic variants modulate ALS–FTD risk and intersect with progranulin-dependent lysosomal biology
- Developed a model system of TMEM106B aggregation that leads to intra-lysosomal fibril formation in human neurons
- Evidence that TMEM106B aggregation induces elevated levels of phospho-TDP-43
- Direct co-localization of TMEM106B fibrils and TDP-43 aggregates within individual lysosomes
- Implications of TMEM106B-driven lysosomal failure as an upstream, targetable mechanism across neurodegenerative diseases