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. 2015 May 28;15(2):e157–e170.

Figure 3:

Figure 3:

Simplified illustration of a scenario modelling the role of DAMPs in ER stress/UPR-mediated, NLRP3-promoted neuroinflammation and neuronal cell death in Alzheimer’s disease.

ER = endoplasmic reticulum; UPR = unfolded protein response; NLRP3 = nucleotide binding oligomerization domain (NOD)-like receptor (NLR)-containing pyrin domain 3; ROS = reactive oxygen species; IL-1β = interleukin-1β; Aβ = amyloid β; TAU = Tau protein; Ca2+ = calcium ion; PERK = protein kinase-like eukaryotic initiation factor 2-alpha kinase; IRE1α = inositol-requiring transmembrane kinase/endoribonuclease 1α; ATF6 = activating transcription factor 6; proIL-1β = prointerleukin-1β; TLRs = Toll-like receptors; HMGB1 = high-mobility group box 1; HSPs = heat shock proteins.