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Fig. 4: Illustration of cytokine-mediated neuroinflammatory pathways linking gut–brain a...
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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
▸Metadata
| doi | |
| pmid | 41569436 |
| pmcid | PMC12891327 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig4_HTML.jpg', 'type': 'external', 'tracked_at': '2026-04-11T18:50:11.764093'} |
| caption | 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 (S |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig4_HTML.jpg |
| image_path | |
| description | |
| figure_label | Fig. 4 |
| figure_number | 4 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
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