ArticleThe Journal of experimental medicine2022
The dense-core plaques of Alzheimer's disease are granulomas.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Feasibility of Using Magnetic Resonance Spectroscopy Test Biomarkers to Diagnose Alzheimer's Disease: Systematic Evaluation and Meta-Analysis.Actas espanolas de psiquiatria · 2024Pooled it
- DeepPlaque: a scalable multimodal platform for Aβ pathology and cell analysis in Alzheimer's disease.EMBO molecular medicine · 2026Article
- Microglia in Alzheimer's Disease: From Homeostatic Guardians to Multifaceted Drivers of Neuropathology.Cells · 2026Review
- Basic Microglial Functions and How They Go Awry in Neurodegenerative Disease.Annual review of pathology · 2026Review
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Identification of novel neuraminidase 1 modulators as potential therapeutics for Alzheimer's disease using virtual screening and molecular dynamics simulations.Scientific reports · 2025Article
- Article
- Intranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice.Journal of Alzheimer's disease : JAD · 2025Article
- Supplementation with fish oil reduces αβ 42 burden and shifts αβ precursor protein processing toward non-amyloidogenic pathways in a rat model of hyperglycaemic Alzheimer's disease.Journal of nutritional science · 2025Article
- Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer's disease.Acta neuropathologica · 2024Article
- Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer's disease.Nature neuroscience · 2024Article
- The TAM Subfamily of Receptor Tyrosine Kinases: The Early Years.International journal of molecular sciences · 2024Review
- Autosomal Dominant Alzheimer's Disease Mutations in Human Microglia Are Not Sufficient to Trigger Amyloid Pathology in WT Mice but Might Affect Pathology in 5XFAD Mice.International journal of molecular sciences · 2024Article
- Increased cysteinyl-tRNA synthetase drives neuroinflammation in Alzheimer's disease.Translational neurodegeneration · 2024Article
- Regulation of brain endothelial cell physiology by the TAM receptor tyrosine kinase Mer.Communications biology · 2023Article
- Enhanced microglial dynamics and paucity of tau seeding in the amyloid plaque microenvironment contributes to cognitive resilience in Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Inflammatory panel cytokines are elevated in the neocortex of late-stage Alzheimer's disease but not Lewy body dementias.Journal of neuroinflammation · 2023Article
- Oxytocin attenuates microglial activation and restores social and non-social memory in APP/PS1 Alzheimer model mice.iScience · 2023Article
- Definition of the contribution of an Osteopontin-producing CD11cProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Vascular-Immune Hypothesis of Alzheimer's Disease.Biomedicines · 2023Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Dense-core plaques, whose centers contain highly polymerized and compacted aggregates of amyloid β peptides, are one of the two defining histopathological features of Alzheimer's disease. Recent findings indicate that these plaques do not form spontaneously but are instead constructed by microglia, the tissue macrophages of the central nervous system. We discuss cellular, structural, functional, and gene expression criteria by which the microglial assembly of dense-core plaques in the Alzheimer's brain parallels the construction of granulomas by macrophages in other settings. We compare the genesis of these plaques to the macrophage assembly of mycobacterial granulomas, the defining histopathological features of tuberculosis. We suggest that if dense-core plaques are indeed granulomas, their simple disassembly may be contraindicated as an Alzheimer's therapy.
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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 OpenQuestion graph.