ReviewFrontiers in immunology2022
The Specific Mechanism of TREM2 Regulation of Synaptic Clearance in Alzheimer's Disease.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Alzheimer's Disease as a Disorder of Neuroimmune Dysregulation.Neurology international · 2026Review
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release.Journal of neuroinflammation · 2026Article
- Targeting Microglial Phagocytosis for Alzheimer's Disease Management: Natural, Pharmacological, Nanoparticle, and Gene Therapy Approaches.CNS & neurological disorders drug targets · 2026Review
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
- Designing Neural Dynamics: From Digital Twin Modeling to Regeneration.International journal of molecular sciences · 2025Review
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- LRRK2 deficiency mitigates amyloid β deposition-mediated pathology in a murine Alzheimer's disease model by reprogramming microglia.Translational psychiatry · 2025Article
- Circulatory extracellular vesicles transport complement C1q for promoting neuronal amyloid-β production in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Amelioration of signaling deficits underlying metabolic shortfall in TREM2The FEBS journal · 2025Article
- Single-microglia transcriptomic transition network-based prediction and real-world patient data validation identifies ketorolac as a repurposable drug for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A Computational Approach in the Systematic Search of the Interaction Partners of Alternatively Spliced TREM2 Isoforms.International journal of molecular sciences · 2024Article
- The interrelationships of CSF sTREM2, AD pathology, minimal depressive symptoms, and cognition in non-demented adults.Alzheimer's research & therapy · 2024Article
- The Importance of Complement-Mediated Immune Signaling in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2024Review
- Dysregulated C1q and CD47 in the aging monkey brain: association with myelin damage, microglia reactivity, and cognitive decline.Frontiers in immunology · 2024Article
- Soluble TREM2 Concentrations in the Cerebrospinal Fluid Correlate with the Severity of Neurofibrillary Degeneration, Cognitive Impairment, and Inflammasome Activation in Alzheimer's Disease.Neurology international · 2023Article
- Microglia as a cellular target of diclofenac therapy in Alzheimer's disease.Therapeutic advances in neurological disorders · 2023Review
- C1q and central nervous system disorders.Frontiers in immunology · 2023Review
- Recent advances in the use of CRISPR/Cas for understanding the early development of molecular gaps in glial cells.Frontiers in cell and developmental biology · 2022Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease. Synaptic dysfunction is an integral feature of AD pathophysiology and a significant factor in early cognitive impairment in AD. Microglia, which are intrinsic immune cells in the central nervous system, play important regulatory roles in the process of synapse formation. Microglia can refine synaptic connections through synaptic clearance to ensure accurate synaptic transmission. Synaptic clearance is not only existed during central nervous system development but also aberrantly activated during AD pathology. However, the mechanisms of synaptic clearance in AD remain to be investigated. TREM2 is involved in the synaptic clearance of microglia, acting alone or with other molecules, such as apolipoprotein E (APOE). In addition, C1q is essential for microglia-mediated synaptic clearance. In this review, we systematically summarized the potential mechanisms of microglia involved in synaptic clearance, comprehensively reviewed the role of TREM2 in microglia regulating synaptic clearance and proposed our hypothesis that TREM2 interacts with APOE and C1q to promote synaptic clearance. This review provides new insights into the role of TREM2 regulation in microglia synaptic clearance and provides potential prospects for the treatment of AD.
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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.