🖼
Fig. 5: Molecular mechanism of NLRP3 inflammasome activation in Alzheimer’s disease (AD)...
active
paper figure
Created: 2026-04-11T11:50:11
By: paper_figures_pipeline
Quality:
95%
🔗 External
ID: paper-fig-41569436-5
Fig. 5Figure 5
Molecular mechanism of NLRP3 inflammasome activation in Alzheimer’s disease (AD). The schematic depicts the two-step activation process: (1) Priming (Signal 1) via TLR/NF-κB signaling upregulates NLRP3 and pro-IL-1β; (2) Activation (Signal 2) occurs upon exposure to Aβ oligomers, ATP, ROS, lysosomal rupture, or mitochondrial dysfunction, leading to NLRP3 oligomerization, ASC speck formation, and caspase-1 activation. Active caspase-1 cleaves pro-IL-1β and pro-IL-18 into mature cytokines and processes gasdermin D (GSDMD) to form membrane pores, inducing pyroptosis. The downstream effects include glial activation, impaired Aβ clearance, tau hyperphosphorylation, and neuronal death, forming a self-amplifying neuroinflammatory loop central to AD pathogenesis
▸Metadata
| doi | |
| pmid | 41569436 |
| pmcid | PMC12891327 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig5_HTML.jpg', 'type': 'external', 'tracked_at': '2026-04-11T18:50:11.782942'} |
| caption | Molecular mechanism of NLRP3 inflammasome activation in Alzheimer’s disease (AD). The schematic depicts the two-step activation process: (1) Priming (Signal 1) via TLR/NF-κB signaling upregulates NLRP |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig5_HTML.jpg |
| image_path | |
| description | |
| figure_label | Fig. 5 |
| figure_number | 5 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
1
0 supporting
0 contradicting
0 neutral
Public annotations (0)Annotate on Hypothes.is →
No public annotations yet.