Lisa Diez

This study shows how Tau condensates age into elastic networks with inhomogeneous polymerization and seed formation, providing mechanistic insight into their transition to pathological aggregates.

This study shows that IgLON5 autoantibodies cause neuronal hyperactivity and Tau pathology by clustering cell surface proteins, linking them to neurodegeneration.

This study shows that increased somatodendritic Tau interacts with nuclear envelope proteins, causing nuclear damage and altering gene expression related to AD and tauopathies.

This study shows that 14-3-3ζ binding to phosphorylated Tau reduces its association with microtubules and inhibits aggregation and condensation.

This study shows that Tau condensation, driven by molecular crowding and RNA coacervation, leads to pathological Tau accumulation at the nuclear envelope and affects nucleocytoplasmic transport.