HAL (France)
open access
Mitochondrial Regulation of Microglial Immunometabolism in Alzheimer’s Disease
Alzheimer’s disease (AD) is an age-associated terminal neurodegenerative disease with no effective treatments. Dysfunction of innate immunity is implicated in the pathogenesis of AD, with genetic studies supporting a causative role in the disease. Microglia, the effector cells of innate immunity in
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- Neuron-derived mitochondrial DNA (mtDNA) activates microglia via the Z-DNA binding protein 1 (ZBP1)-mediated pathway in mild traumatic brain injury.#1288
- Opposing and antagonizing effects of SARS-CoV-2/COVID-19 infection and recombinant zoster vaccination on the risk of late-onset Alzheimer disease#200178
- Endothelial NAD(+) depletion drives vascular senescence and neuroinflammation via mtDNA-cGAS/STING-CD38 signaling in Alzheimer's disease.#135725
- Development of a serum-based microRNA panel for Alzheimer's disease diagnosis.#334740
- Methodological approaches to account for assay changes in longitudinal biomarker analysis: insights from Alzheimer’s blood biomarkers in the MEMENTO cohort#280350
Record · ID 1203919
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive