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. 2021 Dec 7;10:49. doi: 10.1186/s40035-021-00273-y

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Pathogenic mechanisms of lipopolysaccharides (LPS) in Alzheimer’s disease. LPS is a characteristic component in the cell wall of gram-negative bacteria and plays a key role in triggering inflammatory response and initiating and promoting AD pathology. LPS promotes the production of Aβ through the increase of β- and γ-secretases and decrease of α-secretase, and stimulates the accumulation of Aβ. LPS induces the impairment of low-density lipoprotein receptor-related protein-1 (LRP-1), which plays a pivotal role in Aβ clearance. LPS is involved in tau phosphorylation, and accelerates the aggregation of phosphorylated tau. LPS activates the microglial TLR4, RAGE, and TREM2 receptors, inducing release of pro-inflammatory cytokines. LPS activation of the TLR4 signaling pathway and LPS entry in the brain through OMV can induce neuronal cell death. ApoER2: apolipoprotein E receptor 2; BBB: blood–brain barrier; IL-6: interleukin 6; IL-1β: interleukin 1 β; LRP-1: low-density lipoprotein receptor-related protein 1; MBP: myelin basic protein; MMP8: matrix metalloproteinase-8; MyD88: myeloid differentiation primary response 88; NF-κβ: nuclear factor kappa β; NFT: neurofibrillary tangles; NLRP1: Nod-like receptor protein 1; OMV: outer membrane vesicle; PHF: paired helical filament; RAGE: receptor for advanced glycation end products; SCFA: short-chain fatty acid; SR-B1: scavenger reception class B type 1; TLR4: Toll-like receptor 4; TNF-α: tumor necrosis factor α; TREM2: triggering receptor expressed on myeloid cells 2; TRIF: Toll/interleukin-1 receptor-domain-containing adapter-inducing interferon-β; VacA: vacuolating cytotoxin A; VCAM1: vascular cell adhesion molecules-1