Neuroinflammation induced by the peptide amyloid-β (25-35) increase the presence of galectin-3 in astrocytes and microglia and impairs spatial memory

Galectins are animal lectins that bind to beta-galactosides, such as lactose and N-acetyllactosamine, contained in glycoproteins or glycolipids. Galectin-1 (Gal-1) and Galectin-3 (Gal-3) are involved in pathologies associated with the inflammatory process, cell proliferation, adhesion, migration, and apoptosis. Recent evidence has shown that the administration of Amyloid-beta 25-35 (A beta(25-35)) into the hippocampus of rats increases the inflammatory response that is associated with memory impairment and neurodegeneration. Galectins could participate in the modulation of the neuroinflammation induced by the A beta(25-35). The aim of this study was to evaluate the presence of Gal-1 and Gal-3 in the neuroinflammation induced by administration of A beta(25-35) into the hippocampus and to examine spatial memory in the Morris water maze. After the administration of A beta(25-35), animals were tested for learning and spatial memory in the Morris water maze. Behavioral performance showed that A beta(25-35) didn't affect spatial learning but did impair memory, with animals taking longer to find the platform. On the day 32, hippocampus was examined for astrocytes (GFAP), microglia (Iba1), Gal-1 and Gal-3 via immunohistochemical analysis, and the cytokines IL-1 beta, TNF-alpha, IFN-gamma by ELISA. This study's results showed a significant increase in the expression of Gal-3 in the microglia and astrocytes, while Gal-1 didn't increase in the dorsal hippocampus. The expression of galectins is associated with increased cytokines in the hippocampal formation of A beta(25-35) treated rats. These findings suggest that Gal-3 could participate in the inflammation induced by administration of A beta(25-35) and could be involved in the neurodegeneration progress and memory impairment.