Galectin-1 improves cognition and reduces Amyloid-β deposits in an animal model of Alzheimer?s disease possibly by modulating microglia phenotype and increasing Aβ clearance

VINUESA A; GREGOSA A; RABINOVICH G; PRESA JL; BENTIVEGNA M; BEAUQUIS J; SARAVIA F; POMILIO C; ALAIMO A; KWANG SK

Daegu

Congreso; The 10th International Brain Research Organization (IBRO) World Congress of Neuroscience; 2019

International Brain Research Organization (IBRO)

Alzheimer´s disease (AD) is the most common form of dementia associated with an imbalanced production and clearance of amyloid-β peptides (Aβ). Amyloid deposition and neuroinflammation are recognized hallmarks in AD, affecting mainly brain cortex and hippocampus, in addition to microvascular alterations and dysfunction of the blood-brain barrier (BBB). The glycan-binding protein galectin-1 (Gal1) modulates immune and endothelial cells in nervous system compartments, where a neuroprotective role was proposed in autoimmune encephalomyelitis. We study the impact of Gal1 on the cognitive and histopathological state of AD mice. We administered Gal1 (9 i.p. injections of 100 ug/dose) or vehicle during 3 weeks to 12 months-old PDAPPJ20 transgenic mice, or non-transgenic controls. The Gal1 treated group significantly improved cognitive response in the Novel Object Location Recognition test (p