ArticleJournal of neuroinflammation2024
AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed.
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- AIBP deficiency drives MAFLD advancement via ITGβ3 mediated lipid metabolism disruption and pro-inflammatory activation.Cell communication and signaling : CCS · 2026Article
- Increased atherosclerosis and expression of inflammarafts in macrophage foam cells in AIBP-deficient mice.Scientific reports · 2026Article
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- AKAP1 regulates mitochondrial and synaptic homeostasis to enable neuroprotection and repair in retinal ganglion cell degeneration.bioRxiv : the preprint server for biology · 2025Article
- Progressive Loss of Astrocytic AIBP Expression during Alzheimer's Disease Pathology.bioRxiv : the preprint server for biology · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- The Role of APOA-I in Alzheimer's Disease: Bridging Peripheral Tissues and the Central Nervous System.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Amyloid β-Induced Inflammarafts in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Environmental Toxicants and Their Disruption of Integrin Signaling in Lipid Rafts.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Biomarkers in glioblastoma and degenerative CNS diseases: defining new advances in clinical usefulness and therapeutic molecular target.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Microglia-driven neuroinflammation plays an important role in the development of Alzheimer's disease. Microglia activation is accompanied by the formation and chronic expression of TLR4 inflammarafts, defined as enlarged and cholesterol-rich lipid rafts serving as an assembly platform for TLR4 dimers and complexes of other inflammatory receptors. The secreted apoA-I binding protein (APOA1BP or AIBP) binds TLR4 and selectively targets cholesterol depletion machinery to TLR4 inflammaraft-expressing inflammatory, but not homeostatic microglia. Here we demonstrated that amyloid-beta (Aβ) induced formation of TLR4 inflammarafts in microglia in vitro and in the brain of APP/PS1 mice. Mitochondria in Apoa1bp
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Registered trials
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.