ReviewBiochemical pharmacology2014
TREM2 and the neuroimmunology of Alzheimer's disease.
Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 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
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
128 citing papers in PubMed, 219 citations in OpenAlex.
- TREM2-Targeting peptide tracer for neuroinflammation PET imaging.European journal of nuclear medicine and molecular imaging · 2026Article
- Cyclosporine A Modulates Neuroinflammation-Related Gene Expression Associated with Alzheimer's Disease in SH-SY5Y Neuronal Cell Line: Is Cyclosporine A Beneficial/Detrimental?Biochemical genetics · 2026Article
- Cellular signatures of melanocortin pathway genes across the locus coeruleus.Acta neuropathologica communications · 2026Article
- Harnessing the microbiome to regulate myeloid TREM2 expression and innate immune responses.ImmunoHorizons · 2026Article
- Should ApoE4 gene editing therapy be approached with caution when AD is accompanied by retinal neurodegenerative diseases?Frontiers in neurology · 2026Review
- The tango of immune and neural cells: orchestrating neuroinflammation mediated brain disorders.Frontiers in immunology · 2026Review
- Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2025Review
- Article
- Review
- Microglia/Macrophages in Autoimmune Demyelinating Encephalomyelitis (Multiple Sclerosis/Neuromyelitis Optica).International journal of molecular sciences · 2025Review
- Vagus nerve stimulation (VNS) preventing postoperative cognitive dysfunction (POCD): two potential mechanisms in cognitive function.Molecular and cellular biochemistry · 2025Review
- A review on gut microbiota and miRNA crosstalk: implications for Alzheimer's disease.GeroScience · 2025Review
- Alcohol Use Disorder and the Gut-Brain Axis: A Narrative Review of the Role of Gut Microbiota and Implications for Treatment.Microorganisms · 2025Review
- Microglial Modulation in Alzheimer's Disease: Central Players in Neuroinflammation and Pathogenesis.Current Alzheimer research · 2025Review
- Untangling the Genetic Threads of Alzheimer's: Insights into Risk Factors and Biomarkers.Current gene therapy · 2025Review
- PU.1 dictates β-amyloid-induced TREM2 expression upregulation in microglia in a transgenic model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Differential Expression of Neurodegeneration-Related Genes in SH-SY5Y Neuroblastoma Cells Under the Influence of Cyclophilin A: Could the Enzyme be a Likely Trigger and Therapeutic Target for Alzheimer's Disease?Neurochemical research · 2024Article
- Pros and Cons of Human Brain Organoids to Study Alzheimer's Disease.Aging and disease · 2024Review
- Neuroinflammatory Biomarkers in Alzheimer's Disease: From Pathophysiology to Clinical Implications.International journal of molecular sciences · 2024Review
- Amyloid-Beta, Tau, and Microglial Activation in Aged Felid Brains.The Journal of comparative neurology · 2024Article
68 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Late-onset Alzheimer's disease (AD) is a sporadic disorder with increasing prevalence in aging. The ɛ4 allele of Apolipoprotein E(ApoEɛ4) was the only known major risk factor for late onset AD. Recently, two groups of investigators independently identified variants of the TREM2 gene, encoding triggering receptor expressed on myeloid cells 2 as causing increased susceptibility to late onset AD with an odds ratio similar to that of ApoEɛ4. TREM2 is a receptor expressed on innate immune cells. Using a novel technology called Direct RNA Sequencing wedetermined the quantitative transcriptome of microglia, the principal innate neuroimmune cells and confirmed that TREM2 is a major microglia-specific gene in the central nervous system. Over the past several years we have shown that microglia play a dichotomous role in AD. Microglia can be protective and promote phagocytosis, degradation and ultimately clearance of Aβ, the pathogenic protein deposited in the brains of Alzheimer's patients. However, with disease progression, microglia become dysfunctional, release neurotoxins, lose their ability to clear Aβ and produce pro-inflammatory cytokines that promote Aβ production and accumulation. TREM2 has been shown to regulate the phagocytic ability of myeloid cells and their inflammatory response. Here we propose that the mechanism(s) by which TREM2 variants cause Alzheimer's disease are via down regulation of the Aβ phagocytic ability of microglia and by dysregulation of the pro-inflammatory response of these cells. Based on our discussion we propose that TREM2 is a potential therapeutic target for stopping ordelaying progression 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.