Galectin-1-induced cognitive improvement, lower vascular and parenchymal amyloid deposition and immunomodulation in an animal model of Alzheimer?s disease.

POMILIO C; BEAUQUIS J; VINUESA A; BENTIVEGNA M; PRESA J; MORALES R; RABINOVICH G; SARAVIA F

Berlín

Congreso; Berlin BRAIN & BRAIN PET 2017; 2017

International Society for cerebral Blood Flow and Metabolism

Alzheimer?s disease (AD) is the leading cause of dementia in the elderly. Amyloid deposition and neuroinflammation are recognized hallmarks in AD, affecting mainly the brain cortex and hippocampus, both in patients and animal models. Galectin-1 (Gal1) ?a glycan binding protein- is proposed to modulate several properties on immune and endothelial cells. Rabinovich?s group (1) has previously reported a Gal1 neuroprotective role through deactivation of microglia in experimental autoimmune encephalitis, inducing an alternative phenotype. Here, we administered Gal1 or vehicle (i.p. 9 injections of 100ug/dose) during 3 weeks to 12-month-old PDAPPJ20 transgenic mice (Tg), or age-matched non-transgenic animals. Gal1 treatment improved the performance in the novel object location recognition test (p