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

Figure 4

Role of inflammation on Tau pathology: inflammatory stimuli activate the microglial cells and trigger production of proinflammatory cytokines and Tau accumulation in the AD brain. Proinflammatory mediators such as TNF-α (tumor necrosis factor), IL-1β (interleukin-1β), and IL-6 (interleukin-6) could trigger neuroinflammation and tau pathology. Neuroinflammatory response activates a signaling cascade with the release and activation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), overproduction of proinflammatory cytokines, and the activation of neuronal receptors. Hyperphosphorylation of tau protein initiates the dissociation of microtubule. Soluble tau aggregates into pathological tau oligomers, forms tau filaments, and ultimately leads to the formation of neurofibrillary tangles, which promote the neuronal death (created with http://BioRender.com/).