Inflammation and Alzheimer’s Disease: Mechanisms and Therapeutic Implications by Natural Products

Figure 3

Other mechanisms driving neuroinflammation: increased oxidative stress either by excessive production and release of ROS (reactive oxygen species) of inflammatory mediators leading to the overproduction proinflammatory cytokines. Proinflammatory factors activate the glial cells and promote the process of neuroinflammation. Several antioxidants including SOD (superoxide dismutase), Cat (catalase), and GPx (glutathione peroxidase) may act as reducing agents in attenuating ROS production and diminish the inflammatory response. Activated glial cells under the influence of several proinflammatory cytokines trigger the complement system, and the released cytokines form T cells. Activated glial cells further promote the release and activation of inflammatory cytokines such as TNF-α (tumor necrosis factor), IL-1β (interleukin-1β), IL-6 (interleukin-6), NO (nitric oxide), COX-2 (cyclooxygenase-2), IFN-γ (interferon gamma), and chemokines which cause damage to the neurons and lead to their degeneration.