Relevant role of Galectin 1 on experimental Alzheimer´s disease. Effect of treatment on amyloid deposition, neurovascular unit and cognitive performance.

CARLOS POMILIO; JUAN BEAUQUIS; ÁNGELES VINUESA; MELISA BENTIVEGNA; DAVID CLAUSER; ROSA MORALES; GABRIEL RABINOVICH; FLAVIA SARAVIA

Congreso; Congreso Anual de la Sociedad Argentina de Investigaciones Clínicas; 2016

Alzheimer´s disease (AD) is the leading cause of dementia in the elderly. Amyloid deposits and neurofibrillary tangles are among the principal hallmarks in cortex and hippocampus, brain target areas of this devastating disease without effective cure. Neuroinflammation early compromise the components of the neurovascular unit in AD. Galectin-1 (Gal 1) is a glican binding protein which is proposed to have several properties on immune and endothelial cells in the periphery and also in the central nervous system. We found that the astrocytes surrounding the plaques were Gal1+ in the hippocampus of PDAPPJ20 mouse, transgenic (Tg) model of AD. Then, we administered i.p. Gal1 (9 injections of 100ug)/vehicle during 3 weeks to 12 months of age Tg mice, when they exhibited evident plaque deposition. Age-matched non-transgenic mice were used as controls. Gal1 treated group improved the performance in Novel Object Location recognition test, cognitive behavioral test, compared with vehicle group. The plaque load, assessed as Congo Red + area on hippocampal slices, diminished in a significant manner in Gal1 treated mice, reaching almost 70% decrease (p