The Role of Oxidative Stress-Induced Epigenetic Alterations in Amyloid-β Production in Alzheimer’s Disease

Figure 1

The role of amyloidogenesis in Alzheimer’s disease. Amyloid-β originates as amyloid-beta precursor protein in the plasma membrane, which is cleaved sequentially by beta-site APP cleaving enzyme 1 and gamma-secretase. Following interaction between receptors for advanced glycation end products, which leads to its uptake in the brain, amyloid-β can form insoluble plaques and induce neurofibrillary tangles in neurons, the hallmarks of Alzheimer’s disease. Aβ, amyloid-β; AICD, amyloid intracellular domain; APP, amyloid-beta precursor protein; BACE1, beta-site APP cleaving enzyme 1; BBB, blood-brain barrier; C99, residual 99 amino acids from C-terminal of APP; ECF, extra cellular fluid; p38 MAPK, p38 mitogen-activated protein kinase; OS, oxidative stress; PS1, presenilin 1; NFT, neurofibrillary tangle; RAGE, receptor for advanced glycation end products; RBC, red blood cell.