Antonio Boza‐Serrano

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

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.

This study shows that inflammatory bowel disease (IBD) leads to α-synuclein aggregation in the gut and brain, supporting Braak's hypothesis of Parkinson's disease origin in the enteric nervous system.

This study identifies galectin-3 as a novel endogenous TREM2 ligand that regulates microglial activation and Aβ fibrillation in Alzheimer’s disease.