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Fig. 3: Schematic representation of complement pathway activation in Alzheimer’s disease...
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Created: 2026-04-11T11:50:11
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ID: paper-fig-41569436-3
Fig. 3Figure 3
Schematic representation of complement pathway activation in Alzheimer’s disease (AD). The three complement activation routes, classical (C1q binding to Aβ, tau, or antibody complexes), lectin (Mannose-Binding Lectin [MBL] and its associated MBL-associated serine proteases [MASPs]), and alternative (amplification loop), converge at C3 activation, generating C3a/C5a inflammatory mediators and forming the membrane attack complex (MAC). Excessive activation induces aberrant C1q/C3b-mediated synaptic pruning, microglial and astrocytic activation, and neuronal lysis. Age-related BBB breakdown permits peripheral complement infiltration, while failure of regulatory checkpoints leads to persistent complement-driven neuroinflammation and neurodegeneration in AD
▸Metadata
| doi | |
| pmid | 41569436 |
| pmcid | PMC12891327 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig3_HTML.jpg', 'type': 'external', 'tracked_at': '2026-04-11T18:50:11.742759'} |
| caption | Schematic representation of complement pathway activation in Alzheimer’s disease (AD). The three complement activation routes, classical (C1q binding to Aβ, tau, or antibody complexes), lectin (Mannos |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig3_HTML.jpg |
| image_path | |
| description | |
| figure_label | Fig. 3 |
| figure_number | 3 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
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+0%
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0%
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Outgoing
1
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0 contradicting
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