Figure 8. Schematic representation of the hypothetical influence of age-related neuroinflammation and changes in AKT-GSK-3β and DVL-2/ β-CATENIN signaling in rat hippocampus, increasing susceptibility to neurodegenerative process. All data showed in present manuscript are in color pattern: orange for protein expression in cytosol, except for GSK-3β that has activity level represented, and green for nuclear expression of transcription factors and mRNA. All hypothetical explanations are in grey and were not measured in this paper. The present work showed that age-related increase in neuroinflammation as indicated by NF-кB activation, increase in TNF-α and decrease of IL-10 levels, combined with a basal reduction in the pAKT increasing GSK-3β activity, what can be related to a decrease in DVL-2/β-CATENIN pathway in hippocampus in the presence of high levels of serum GCs, may predispose an effect of specific factor in the manifestation of age-related degenerative disorders. In fact, in response to the neuroinflammatory status and decrease of DVL-2 linked to β-CATENIN pathway in hippocampus, microglia should become activated and high levels of glutamate (GLU) is frequently associated with impaired handling of extracellular GLU by gliotic astrocyte [100–103].