ArticleAnimal models and experimental medicine2025
Microglial ApoD-induced NLRC4 inflammasome activation promotes Alzheimer's disease progression.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Injury-transduced oligodendrocytes modulate neuroinflammation and glial activation in diseased and non-diseased central nervous system.Nature communications · 2026Article
- Tracing neuroinflammation in neurodegeneration: insights from a scoping review on biofluid biomarkers.Brain communications · 2026Review
- ApoD mediates age-associated increase in vulnerability to influenza virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Potential Role of Inflammasomes in Aging.International journal of molecular sciences · 2025Review
- Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old Mice.bioRxiv : the preprint server for biology · 2025Article
- Inflammasome-Mediated Neuroinflammation: A Key Driver in Alzheimer's Disease Pathogenesis.Biomolecules · 2025Review
- Microglial ApoD-induced NLRC4 inflammasome activation promotes Alzheimer's disease progression.Animal models and experimental medicine · 2025Article
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
- The Emerging Evidence for a Protective Role of Fucoidan fromMarine drugs · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is a progressive neurodegenerative disease with no effective therapies. It is well known that chronic neuroinflammation plays a critical role in the onset and progression of AD. Well-balanced neuronal-microglial interactions are essential for brain functions. However, determining the role of microglia-the primary immune cells in the brain-in neuroinflammation in AD and the associated molecular basis has been challenging.
methodsInflammatory factors in the sera of AD patients were detected and their association with microglia activation was analyzed. The mechanism for microglial inflammation was investigated. IL6 and TNF-α were found to be significantly increased in the AD stage.
resultsOur analysis revealed that microglia were extensively activated in AD cerebra, releasing sufficient amounts of cytokines to impair the neural stem cells (NSCs) function. Moreover, the ApoD-induced NLRC4 inflammasome was activated in microglia, which gave rise to the proinflammatory phenotype. Targeting the microglial ApoD promoted NSC self-renewal and inhibited neuron apoptosis. These findings demonstrate the critical role of ApoD in microglial inflammasome activation, and for the first time reveal that microglia-induced inflammation suppresses neuronal proliferation.
conclusionOur studies establish the cellular basis for microglia activation in AD progression and shed light on cellular interactions important for AD treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.