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Fig. 4: Illustration of cytokine-mediated neuroinflammatory pathways linking gut–brain a...

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paper figure Created: 2026-04-11T11:50:11 By: paper_figures_pipeline Quality: 95% 🔗 External ID: paper-fig-41569436-4
Fig. 4: Illustration of cytokine-mediated neuroinflammatory pathways linking gut–brain a...
Fig. 4Figure 4
Illustration of cytokine-mediated neuroinflammatory pathways linking gut–brain axis (GBA) dysfunction to Alzheimer’s disease (AD) pathology. Gut microbiota dysbiosis reduces short-chain fatty acids (SCFAs) and increases intestinal permeability, facilitating lipopolysaccharide (LPS) leakage into circulation and blood–brain barrier (BBB) disruption. Translocated LPS activates glial cells and promotes pro-inflammatory cytokine release (IL-1β, TNF-α, IL-6, IL-8, IFN-γ) through NF-κB, NLRP3, RAGE, and TRAIL signaling, leading to Aβ plaque deposition, tau hyperphosphorylation, and neuronal injury. In contrast, anti-inflammatory cytokines (IL-4, IL-10, TGF-β, IL-2, IL-3) modulate immune homeostasis via TREM2, PD-1/PD-L1, PI3K/Akt/mTOR, and cGAS–STING pathways. The imbalance between these signaling cascades drives chronic neuroinflammation and accelerates AD progression. Aβ amyloid-β, NF-κB nuclear factor kappa B, NLRP3 NOD-like receptor protein 3, RAGE receptor for advanced glycation end-prod
PubMed: 41569436
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doi
pmid41569436
pmcidPMC12891327
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captionIllustration of cytokine-mediated neuroinflammatory pathways linking gut–brain axis (GBA) dysfunction to Alzheimer’s disease (AD) pathology. Gut microbiota dysbiosis reduces short-chain fatty acids (S
image_urlhttps://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig4_HTML.jpg
image_path
description
figure_labelFig. 4
figure_number4
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source_strategypmc_api
entities_mentioned
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