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Fig. 2: Schematic representation of astrocytic activation and neuroinflammatory pathways...
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Created: 2026-04-11T11:50:11
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ID: paper-fig-41569436-2
Fig. 2Figure 2
Schematic representation of astrocytic activation and neuroinflammatory pathways in Alzheimer’s disease (AD). Exposure to amyloid-β (Aβ) or injury triggers reactive astrocytosis with increased GFAP, vimentin, and nestin expression, leading to neurotoxic or neuroprotective phenotypes. Activated astrocytes release nitric oxide (NO) via iNOS and monoamine oxidase-B (MAO-B), producing excessive γ-aminobutyric acid (GABA) and gliotransmitters (GABA, glutamate, ATP), disrupting neuronal signaling and impairing memory. Microglial activation, ROS generation, and NF-κB signaling further exacerbate neurodegeneration and Aβ plaque accumulation. ATP adenosine triphosphate, GABA γ-aminobutyric acid, GFAP glial fibrillary acidic protein, iNOS inducible nitric oxide synthase, MAO-B monoamine oxidase-B, NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells, NO nitric oxide, ROS reactive oxygen species
▸Metadata
| doi | |
| pmid | 41569436 |
| pmcid | PMC12891327 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig2_HTML.jpg', 'type': 'external', 'tracked_at': '2026-04-11T18:50:11.720339'} |
| caption | Schematic representation of astrocytic activation and neuroinflammatory pathways in Alzheimer’s disease (AD). Exposure to amyloid-β (Aβ) or injury triggers reactive astrocytosis with increased GFAP, v |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12891327/bin/10571_2026_1671_Fig2_HTML.jpg |
| image_path | |
| description | |
| figure_label | Fig. 2 |
| figure_number | 2 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
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