ReviewFrontiers in neurology2018
Microglia in Alzheimer's Disease: Risk Factors and Inflammation.
Review in Frontiers in neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed.
- Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer's disease.Nature aging · 2021Trial
- Trace Elements Dyshomeostasis and Toxic Metals Neurotoxicity in Neurodegenerative Diseases.Biological trace element research · 2026Review
- The emerging role of circular RNAs in neurodegenerative diseases and viral infections.Journal of neurovirology · 2026Review
- Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Intracerebroventricular streptozotocin-induced animal model of Alzheimer's disease: revealing dose optimization, administration regimen, and molecular pathways.Laboratory animal research · 2026Review
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Emerging roles of circular RNAs and enhancer RNAs: new insights into the development and management of neurodegenerative disorders.Biomarker research · 2026Review
- Microglia networks within the tapestry of alzheimer's disease through spatial transcriptomics.Molecular neurodegeneration · 2025Review
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- Psychoactive substances: novel molecular insights and therapeutic potential for Alzheimer's disease.Translational neurodegeneration · 2025Review
- Role of Oxidative Stress and Neuroinflammation in the Etiology of Alzheimer's Disease: Therapeutic Options.Antioxidants (Basel, Switzerland) · 2025Review
- Ligand-Receptor Analysis of Brain Cell Type Marker Data Reveals Intricate Endothelial Interaction.Annals of neurosciences · 2025Article
- Microglial TLR4-Lyn kinase is a critical regulator of neuroinflammation, Aβ phagocytosis, neuronal damage, and cell survival in Alzheimer's disease.Scientific reports · 2025Article
- Co-regulation of microglial subgroups in Alzheimer's amyloid pathology: Implications for diagnosis and drug development.PloS one · 2025Article
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
- Network dynamics-based subtyping of Alzheimer's disease with microglial genetic risk factors.Alzheimer's research & therapy · 2024Article
- Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.Neurobiology of aging · 2024Article
- Single-Cell RNA Sequencing Reveals Immunomodulatory Effects of Stem Cell Factor and Granulocyte Colony-Stimulating Factor Treatment in the Brains of Aged APP/PS1 Mice.Biomolecules · 2024Article
- An overview on microglial origin, distribution, and phenotype in Alzheimer's disease.Journal of cellular physiology · 2024Review
- SKA2 regulated hyperactive secretory autophagy drives neuroinflammation-induced neurodegeneration.Nature communications · 2024Article
17 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are resident immune cells in the central nervous system (CNS) that originate from myeloid progenitor cells in the embryonic yolk sac and are maintained independently of circulating monocytes throughout life. In the healthy state, microglia are highly dynamic and control the environment by rapidly extending and retracting their processes. When the CNS is inflamed, microglia can give rise to macrophages, but the regulatory mechanisms underlying this process have not been fully elucidated. Recent genetic studies have suggested that microglial function is compromised in Alzheimer's disease (AD), and that environmental factors such as diet and brain injury also affect microglial activation. In addition, studies of triggering receptor expressed on myeloid cells 2-deficiency in AD mice revealed heterogeneous microglial reactions at different disease stages, complicating the therapeutic strategy for AD. In this paper, we describe the relationship between genetic and environmental risk factors and the roles of microglia in AD pathogenesis, based on studies performed in human patients and animal models. We also discuss the mechanisms of inflammasomes and neurotransmitters in microglia, which accelerate the development of amyloid-β and tau pathology.
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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.