Fig. 3

Association of AD pathways with miRNAs with potential for diagnostic applications. As one of the key pathological pathways of AD development, Aβ has effects on the development of mitochondrial dysfunction, oxidative stress, and induction of the calcium signaling pathway. The calcium signaling pathway affects the development of apoptosis via lipid oxidation, protein oxidation, and DNA damage, leading to cell death. One of the mechanisms of neuronal damage is represented by hyperphosphorylated Tau protein, which causes neurofibrillary degeneration. The image also shows the effect of inflammatory factors on neuronal damage. TNF, tumor necrosis factor; TNFR, tumor necrosis factor receptor; IKK, IκB kinase; PKR, protein kinase R; JNK, c-Jun N-terminal kinase; RAGE, receptor for advanced glycation endproducts; MEK, mitogen-activated protein kinase; ERK1/2, extracellular signal-regulated kinases; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; IL, interleukin; mTOR, mechanistic target of rapamycin; VDCC, voltage-dependent calcium channel; Cdk5, cyclin dependent kinase 5; PP2B, protein phosphatase-2B; GSK3B, glycogen synthase kinase 3 beta; NMDAR, N-methyl-D-aspartate receptor; NOS, nitric oxide synthase; RyR, ryanodine receptors; PSEN, presenilin; SERCA, sarco/endoplasmic reticulum Ca2+-ATPase; FADD, Fas-associated protein with death domain; BID, BH3 interacting-domain death agonist; CytC, cytochrome complex; APP, amyloid precursor protein; APP-BP1, amyloid precursor protein-binding protein 1; BACE1, beta-site APP cleaving enzyme 1; Cx proteins I-V, electron transport chain enzymes (complexes I-IV) and the ATP synthase (complex V); ABAD, amyloid beta-binding alcohol dehydrogenase; CypD, mitochondrial peptidyl-prolyl cis–trans isomerase D