Christopher M. Henstridge

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

The paper develops novel in vivo TDP-43 stress reporter models to identify early biomarkers for ALS, showing tissue-specific activation in the cerebellum before clinical signs appear.

The paper shows human astrocytes and microglia ingest more synapses in Alzheimer's disease via MFG-E8, and inhibiting MFG-E8 reduces this ingestion in cultured cells.

This study shows that reducing tau with a degrader prevents mitochondrial fragmentation and oxidative stress in ALS models.

This study uses MRI and histology to identify structural and cellular changes in TDP-43 knock-in mice, linking them to ALS-FTD pathology and identifying PV+ interneuron loss as a potential biomarker.

The paper identifies over 5,500 synaptic proteins in Alzheimer’s disease and controls, revealing APOE4-associated changes in synaptic and mitochondrial function and neuroimmune signaling.

This study shows that reducing tau improves behavioural and transcriptional issues in a mouse model of Alzheimer’s disease, suggesting synaptic tau reduction could be a therapeutic strategy.