Sue‐Ann Mok

This study identifies TRAPPC8 as a brake on UFMylation that suppresses tauopathy by interacting with UBA5, showing its therapeutic potential in Alzheimer's disease.

This study uses single-molecule mass photometry to directly observe protein aggregation kinetics and identify inhibitor effects on aggregation mechanisms.

This study identifies a metabolite from E. coli that suppresses tau aggregation in vitro and in live bacteria, suggesting its potential for modulating tauopathies.

This study shows that DAP12 deficiency reduces tau-induced inflammation and myelin loss in mice, despite increased tau pathology, by altering microglia-oligodendrocyte interactions.

This study shows gangliosides modulate EV secretion and misfolded protein cargo, with GM1 enhancing EV release and reducing mutant huntingtin burden in HD models.

This study combines APOE4 and TREM2R47H in female tauopathy mice to identify pathways activated by AD risk factors, finding cGAS-STING signaling and microglial senescence as potential drivers.

The R136S mutation on APOE3 enhances resistance to tau-related pathology and toxicity by downregulating the cGAS-STING-IFN signaling pathway.

The paper creates a human iPSC model of 4R tauopathy and identifies genetic modifiers of Tau propagation using CRISPRi screening.

This study shows that microglial NF-κB signaling drives tau spreading and toxicity in a mouse model of tauopathy, with inhibition reducing tau pathology and cognitive deficits.

The paper maps Tau interactomes in neurons using APEX and AP-MS to reveal activity-dependent interactions and FTD mutation effects on mitochondrial associations in neurodegenerative diseases.

The paper shows that tau conformers in FTLD-MAPT undergo liquid-liquid phase separation and disrupt nuclear envelope function, leading to cell death and fibrillar structures.

This study identifies p300/CBP as a regulator of tau secretion via the autophagy-lysosomal pathway, showing its role in tau propagation in tauopathies.