Jose Luis Venero

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

The paper investigates metabolic and transcriptional changes in microglia after phagocytosis, showing these adaptations sustain their functionality and regenerative properties.

The paper screens FDA-approved drugs to identify modulators of the TREM2-TYROBP transmembrane interaction, finding varenicline as a potential agonist.

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 Galectin-3 depletion reduces immunosuppressive microglia and limits cancer cell growth in brain tumours.

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 Arg1+ microglia as a distinct subtype in female mice, showing their role in cognitive function through dendritic spine maturation and behavior.

This study shows TET2 regulates microglial inflammatory responses through NF-κB-dependent pathways and metabolic changes, suggesting it as a target for neurodegenerative diseases.

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