Emil Axell

This study shows that Galectin-3 promotes tau pathology, neuroinflammation, white matter degeneration, and proteomic dysregulation, and that its deletion reduces these effects.

This study shows that structural defects in amyloid-β fibrils are key sites for secondary nucleation, suggesting new strategies for drug design to inhibit amyloid disorders.

This paper identifies Galectin-3 as a key regulator of amyloid-beta aggregation and microglial dysfunction in Alzheimer's disease, showing its role in neurotoxicity and potential as a therapeutic target.