Figure 1.

Aβ fibrils lead to neuronal death, which include ROS generation, neurotoxicity, release of inflammatory cytokines, and activation of the complement system. Due to the accumulation of Aβ oligomers, neuronal degeneration may stimulate the microglial activation, which will initiate the liberation of proinflammatory mediators, neurotoxins, and free radicals but also play a pivotal role in the elimination of Aβ peptides. These peptides trigger oxidative stress and promote inflammatory processes in neurons, which enhance the production of Aβ peptides via increased APP expression. Activated MAPK (a mitogen-activated protein kinase) and NF-кB (nuclear factor kappa-light-chain-enhancer of activated B cells) lead to the production of proinflammatory cytokines, and their increased expansion promotes APP processing and disintegration of BBB (blood-brain barrier) and aggravates the phosphorylation of Tau protein and eventually leads to the formation of neurofibrillary tangles via the activation of p38-MAPK which leads to neuronal degeneration (created with http://BioRender.com/).