ArticleMolecular immunology2021
TREM2 alters the phagocytic, apoptotic and inflammatory response to Aβ
Article in Molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
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Who cites it
40 citing papers in PubMed.
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- Anticancer Treatment Influences TREM2 in Tumor-Associated Macrophages in Lung Cancer.Cancer research and treatment · 2026Article
- TREM2 in age-related macular degeneration: a microglia-centered perspective in the retinal myeloid landscape.Frontiers in ophthalmology · 2026Review
- Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Mitochondrial immunometabolism in sepsis: orchestrating macrophage polarization and dysfunction.European journal of medical research · 2025Review
- Uric Acid Functions as an Endogenous Modulator of Microglial Function and Amyloid Clearance in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Chronic alcohol consumption induces phenotypic and functional alterations consistent with a hyper-inflammatory state in peripheral blood mononuclear cell-derived microglia in a rhesus macaque model.Brain, behavior, and immunity · 2025Article
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- GM1 Oligosaccharide Modulates Microglial Activation and α-Synuclein Clearance in a Human In Vitro Model.International journal of molecular sciences · 2025Article
- Mutant THAP11 causes cerebellar neurodegeneration and triggers TREM2-mediated microglial activation in mice.The Journal of clinical investigation · 2025Article
- TREM2-mediated regulation of microglial activity: a promising target for the treatment of ischemic stroke.Journal of translational medicine · 2025Review
- Short-Term Inhibition of NOX2 Prevents the Development of Aβ-Induced Pathology in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- The microcirculation, the blood-brain barrier, and the neurovascular unit in health and Alzheimer disease: The aberrant pericyte is a central player.Pharmacological reviews · 2025Review
- An adoptive cell therapy with TREM2-overexpressing macrophages mitigates the transition from acute kidney injury to chronic kidney disease.Clinical and translational medicine · 2025Article
- Detrimental influence of Arginase-1 in infiltrating macrophages on poststroke functional recovery and inflammatory milieu.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Treatment of Alzheimer's Disease subjects with expanded non-genetically modified autologous natural killer cells (SNK01): a phase I study.Alzheimer's research & therapy · 2025Article
- Neuraminidase 1 regulates neuropathogenesis by governing the cellular state of microglia via modulation of Trem2 sialylation.Cell reports · 2025Article
- Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration.Frontiers in cellular neuroscience · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau. Also present are dystrophic neurites, loss of synapses, neuronal death, and gliosis. AD genetic studies have highlighted the importance of inflammation in this disease by identifying several risk associated immune response genes, including TREM2. TREM2 has been strongly implicated in basic microglia function including, phagocytosis, apoptosis, and the inflammatory response to Aβ in mouse brain and primary cells. These studies show that microglia are key players in the response to Aβ and in the accumulation of AD pathology. However, details are still missing about which apoptotic or inflammatory factors rely on TREM2 in their response to Aβ, especially in human cell lines. Given these previous findings our hypothesis is that TREM2 influences the response to Aβ toxicity by enhancing phagocytosis and inhibiting both the BCL-2 family of apoptotic proteins and pro-inflammatory cytokines. Aβ
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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.