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

Figure 2

The role of oxidative stress in the multiple domains of amyloid-β production regulation. Oxidative stress, caused from reactive oxygen species production, creates an environment which is epigenetically, transcriptionally, and translationally favorable for amyloid-β production. Aβ, amyloid-β; APP, amyloid-beta precursor protein; BACE1, beta-site APP cleaving enzyme 1; CAT, catalase; DNMT, DNA methyltransferase; eIF2α, eukaryotic translation initiation factor-2alpha; GPx, glutathione peroxidase; HAT, histone acetyltransferase; HDAC, histone deacetylase complex; JNK, c-Jun N-terminal kinase; p38 MAPK, p38 mitogen-activated protein kinase; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; OS, oxidative stress; PKR, double-stranded RNA dependent protein kinase; PS1, presenilin 1; SOD, superoxide dismutase.