Adam K. Walker

The paper identifies early synaptic vesicle cycle disruption in ALS using proteomics and shows it is reversible with TDP-43 suppression.

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 shows that TDP-43 aggregation in skeletal muscle causes motor dysfunction and neurodegeneration, but clearance of the protein allows for functional recovery.

This study identifies persistent extra-motor behavioural deficits in rNLS8 TDP-43 mice, linked to synaptic gene expression and splicing changes that persist even after motor recovery.

This study shows that microglial morphology changes before immunophenotype shifts in ALS, driven by TDP-43 aggregation, suggesting morphological changes may trigger immunological responses.

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 identifies early activation of stress and apoptotic pathways in a mouse model of ALS/FTD and shows that suppressing Chop has limited effects on disease progression.

This study examines microglial activation and TDP-43 pathology in ALS brains, finding increased CD68 and L-ferritin expression in human and mouse models linked to pTDP-43 aggregation.

This study investigates how RNA-binding deficiency and post-translational modifications of TDP-43 lead to its sequestration and depletion, contributing to neurodegeneration in ALS and FTD.

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

This study shows that TDP-43 mislocalization to the cytoplasm in motor cortex neurons causes hyperexcitability and reduced excitatory neurotransmission, linking early ALS pathology to TDP-43 mislocalization.