Promising role for Galectin 1 in Alzheimer? disease: reduced microglial activation and lower amyloid deposition in the hippocampus together with cognitive improvement after treatment in a transgenic mouse model.

FLAVIA E. SARAVIA; MELISA BENTIVEGNA; GABRIEL RABINOVICH; CARLOS POMILIO; JÉSICA PRESA; JUAN BEAUQUIS; ANGELES VINUESA; ROSA MORALES

Edimburgo

Congreso; Glia Meeting 2017; 2017

Alzheimer?s disease (AD) is the leading cause of dementia in the elderly and there is no treatment available nowadays. 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. G Rabinovich et al reported a Gal1 neuroprotective role through deactivation of microglia in experimental autoimmune encephalitis, inducing a M2 alternative phenotype. Here, we administered Gal1 or vehicle (i.p. 9 injections of 100ug/dose) during 3 weeks to 12 months-old PDAPPJ20 Tg mice, or age-matched non-transgenic animals. Iba1+ microglial cells in the dentate gyrus exhibited less reactivity measured as soma size after Gal1 treatment (p