SynthesisTrends in neurosciences2020
Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics.
Synthesis in Trends in neurosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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.
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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
117 citing papers in PubMed, 234 citations in OpenAlex.
- Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice.Nature communications · 2026Article
- Bidirectional communication between the gut microbiota and the central nervous system.Neural regeneration research · 2026Article
- Blood serum from individuals with Alzheimer's disease alters microglial phagocytosis in vitro.Neural regeneration research · 2026Article
- MEF2C controls lysosomal and lipid clearance programs linked to Alzheimer's disease risk in macrophages.Research square · 2026Article
- Mesenchymal stem cells and secretome as modulators of neuroinflammation in neurological disorders.Journal of translational medicine · 2026Review
- Complement receptor 3 (CR3)-dependent microglial synapse elimination drives Parkinson's disease pathogenesis in systemic inflammation.Cell death & disease · 2026Article
- Extracellular Succinate Modulates Neuroimmune Responses in a Murine Microglial Cell Line.Biomolecules · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration.Nature communications · 2026Article
- Functional border-associated macrophages limit Alzheimer's Disease progression.bioRxiv : the preprint server for biology · 2026Article
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Basic Microglial Functions and How They Go Awry in Neurodegenerative Disease.Annual review of pathology · 2026Review
- Roles of Glia in Synapse Nano-organization.Advances in neurobiology · 2026Review
- Spatial and single-cell transcriptomics reveal the reorganization of cerebellar microglia with aging.Cell reports · 2025Article
- A validated method for banking mixed glial cultures that yield responsive microglia.bioRxiv : the preprint server for biology · 2025Article
- Microglia-derived APOE2 improves remyelination even in the presence of endogenous APOE4.Journal of neuroinflammation · 2025Article
- Dysregulated Resolution of Inflammation After Respiratory Viral Infections: Molecular Pathways Linking Neuroinflammation to Post-Viral Neuropathic Pain-A Narrative Review.International journal of molecular sciences · 2025Review
- DKK3-LRP1 complex and a chemical inhibitor regulate Aβ clearance in models of Alzheimer's disease.Science advances · 2025Article
- Human iPSC-Derived Microglia Integrate Into Cerebral Organoids and Assume an In Vivo-Like Phenotype.The European journal of neuroscience · 2025Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease. Genetic studies involving genome-wide association studies (GWAS) and meta-analysis have discovered numerous genomic loci associated with AD; however, the causal genes and variants remain unidentified in most loci. Integration of GWAS signals with epigenomic annotations has demonstrated that AD risk variants are enriched in myeloid-specific enhancers, implicating myeloid cells in AD etiology. AD risk variants in these regulatory elements modify disease susceptibility by regulating the expression of genes that play crucial roles in microglial phagocytosis. Several of these AD risk genes are specifically expressed in myeloid cells, whereas others are ubiquitously expressed but are regulated by AD risk variants within myeloid enhancers in a cell type-specific manner. We discuss the impact of established AD risk variants on microglial phagocytosis and debris processing via the endolysosomal system.
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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 OpenQuestion graph.