Rachel E. Hodgson

This study identifies TDP-43-independent mechanisms of STMN2 depletion in ALS, showing acute stress causes proteasomal degradation and translational repression, while chronic stress leads to reduced protein levels, with mRNA upregulation as a compensatory mechanism in some subtypes.

This study shows that senescent human cells secrete misfolded proteins via the endo-lysosomal system, driven by DNAJC5 and reduced intracellular proteostasis.

This study shows that FUS RNA condensation regulates its splicing and that disrupting this process can reduce FUS levels, offering a potential therapeutic strategy for ALS-FUS.

This study uses optogenetics to model C9orf72 poly-PR condensation in cells, revealing anisotropic nuclear condensates that cause TDP-43 pathology without stress response activation.