Amyloid-ß (25-35) induces the morphological alteration of dendritic spines and decreases NR2B and PSD-95 expression in the hippocampus.

Research on the memory impairment caused by the Amyloid-ß 25-35 (Aß25-35) peptide in animal models has provided an understanding of the causes that occurs in Alzheimer's disease. However, it is uncertain whether this cognitive impairment occurs due to disruption of information encoding and consolidation or impaired retrieval of stored memory. The aim of this study was to determine the effect of the Aß25-35 peptide on the morphology of dendritic spines and the changes in the expression of NR2B and PSD-95 in the hippocampus associated with learning and memory deficit. Vehicle or Aß25-35 peptide (0.1 µg/µL) was bilaterally administered into the CA1 subfield of the rat hippocampus, then tested for spatial learning and memory in the Morris Water Maze. On Day 39, the morphological changes in the CA1 of the hippocampus and dentate gyrus were examined via Golgi-Cox stain. It was observed that the Aß25-35 peptide administered in the CA1 region of the rat hippocampus induced changes to the morphology of dendritic spines and the expression of the NR2B subunit of the NMDA receptor co-localized with both the spatial memory and PSD-95 protein in the hippocampus of learning rats. We conclude that, in soluble form, the Aß25-35 peptide perturbs synaptic plasticity, specifically in the formation of new synapses, thus promoting the progression of memory impairment.

The therapeutic potential of galectin-1 and galectin-3 in the treatment of neurodegenerative diseases.

Introduction: Neuroinflammation has been proposed as a common factor and one of the main inducers of neuronal degeneration. Galectins are a group of ß-galactoside-binding lectins, that play an important role in the immune response, adhesion, proliferation, differentiation, migration and cell growth. Up to 15 members of the galectin's family have been identified; however, the expression of galectin-1 and galectin-3 has been considered a key factor in neuronal regeneration and modulation of the inflammatory response. Galectin-1 is necessary to stimulate the secretion of neurotrophic factors in astrocytes and promoting neuronal regeneration. In contrast, galectin-3 fosters the proliferation of microglial cells and modulates cellular apoptosis, therefore these proteins are considered a useful alternative for the treatment of degenerative diseases.Areas covered: This review describes the roles of galectin-1 and galectin-3 in the modulation of neuroinflammation and their potential as therapeutic targets in the treatment for neurodegenerative diseases.Expert opinion: Although data in the literature vary, the effects of galectin-1 and galectin-3 on the activation and modulation of astrocytes and microglia has been described. Due to its anti-inflammatory effects, galectin-1 is proposed as a molecule with therapeutic potential, whereas the inhibition of galectin-3 could contribute to reduce the neuroinflammatory response in neurodegenerative diseases.

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

Galectins are animal lectins that bind to ß-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-ß 25-35 (Aß25-35) 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 Aß25-35. The aim of this study was to evaluate the presence of Gal-1 and Gal-3 in the neuroinflammation induced by administration of Aß25-35 into the hippocampus and to examine spatial memory in the Morris water maze. After the administration of Aß25-35, animals were tested for learning and spatial memory in the Morris water maze. Behavioral performance showed that Aß25-35 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-1ß, TNF-α, IFN-γ 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 Aß25-35 treated rats. These findings suggest that Gal-3 could participate in the inflammation induced by administration of Aß25-35 and could be involved in the neurodegeneration progress and memory impairment.