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Fig. 2: Characteristic cGAS-STING pathways in different neurodegenerative diseases. In A...

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paper figure Created: 2026-04-22T16:25:20 By: paper_figures_pipeline Quality: 50% 🔗 External ID: paper-fig-b155478e-45ab-40b5-a0f5-8b740a
Fig. 2: Characteristic cGAS-STING pathways in different neurodegenerative diseases. In A...
Fig. 2Figure 2
Characteristic cGAS-STING pathways in different neurodegenerative diseases. In Alzheimer’s disease, mutations in APOE4 and TREM2 lead to mtDNA leakage by impairing mitochondrial membrane permeability, activating the cGAS-STING pathway and promoting Aβ accumulation. Aβ and tau tangles can further activate this pathway. In Parkinson’s disease, defects in the PINK1, Parkin, and LRRK2 genes cause mtDNA release, activating the cGAS-STING pathway and promoting abnormal α-syn aggregation. α-syn aggregates themselves can induce DNA damage and increase cytosolic DNA accumulation. In ALS, loss of function in the C9ORF72 gene impairs STING degradation; pathogenic TDP-43 and misfolded SOD1 proteins induce mitochondrial dysfunction that promotes leakage of molecules including mtDNA. In Huntington’s disease, mutant mHTT elevates oxidative stress levels, triggers mtDNA leakage, and ultimately activates the cGAS-STING pathway
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doi10.1186/s12974-025-03563-8
pmcidPMC12522239
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captionCharacteristic cGAS-STING pathways in different neurodegenerative diseases. In Alzheimer’s disease, mutations in APOE4 and TREM2 lead to mtDNA leakage by impairing mitochondrial membrane permeability,
paper_idb155478e-45ab-40b5-a0f5-8b740ae54481
image_urlhttps://www.ebi.ac.uk/europepmc/articles/PMC12522239/bin/12974_2025_3563_Fig2_HTML.jpg
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description
figure_labelFig. 2
figure_number2
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source_strategypmc_api
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