ArticleActa neuropathologica2021
TREM2 expression in the brain and biological fluids in prion diseases.
Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association of soluble TREM2 with Alzheimer's disease and mild cognitive impairment: a systematic review and meta-analysis.Frontiers in aging neuroscience · 2024Pooled it
- TREM2-Targeting peptide tracer for neuroinflammation PET imaging.European journal of nuclear medicine and molecular imaging · 2026Article
- Spatial characterisation of TREM2 expression in actively demyelinating multiple sclerosis lesions supports its key roles in lipid metabolic pathways.Acta neuropathologica communications · 2026Article
- Soluble TREM2 Is Elevated in Pediatric Patients with Anti-NMDAR Encephalitis.Journal of clinical medicine · 2026Article
- Connectivity of the adult human brain with sequential neurogenesis of circuits and transcriptomics signatures.Nature communications · 2025Article
- Rapid decline of cerebrospinal fluid biomarkers of axonal injury and neuroinflammation after initiation of antiretroviral therapy in HIV.Journal of neurovirology · 2025Article
- Microglial Activation Visualized by [European journal of neurology · 2025Article
- Biological Fluid Biomarkers in Human Prion Diseases with a Note on Biosafety.Sub-cellular biochemistry · 2025Review
- Biomarkers Unveiling the Interplay of Mind, Nervous System, and Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Review
- A Computational Approach in the Systematic Search of the Interaction Partners of Alternatively Spliced TREM2 Isoforms.International journal of molecular sciences · 2024Article
- Prenatal SARS-CoV-2 infection results in neurodevelopmental and behavioral outcomes in mice.JCI insight · 2024Article
- MoDAFold: a strategy for predicting the structure of missense mutant protein based on AlphaFold2 and molecular dynamics.Briefings in bioinformatics · 2024Article
- Decoding sTREM2: its impact on Alzheimer's disease - a comprehensive review of mechanisms and implications.Frontiers in aging neuroscience · 2024Review
- Methods to Discover and Validate Biofluid-Based Biomarkers in Neurodegenerative Dementias.Molecular & cellular proteomics : MCP · 2023Article
- Genetic analysis of potential biomarkers and therapeutic targets in neuroinflammation from sporadic Creutzfeldt-Jakob disease.Scientific reports · 2023Article
- Soluble TREM2 in body fluid in Alzheimer's disease and Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Emerging Roles of Cells and Molecules of Innate Immunity in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Potential role of TREM2 in high cholesterol‑induced cell injury and metabolic dysfunction in SH‑SY5Y cells.Experimental and therapeutic medicine · 2023Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023Review
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26 authors.
Funding
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Abstract
Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune cell surface receptor that regulates microglial function and is involved in the pathophysiology of several neurodegenerative diseases. Its soluble form (sTREM2) results from shedding of the TREM2 ectodomain. The role of TREM2 in prion diseases, a group of rapidly progressive dementias remains to be elucidated. In the present study, we analysed the expression of TREM2 and its main sheddase ADAM10 in the brain of sporadic Creutzfeldt-Jakob disease (sCJD) patients and evaluated the role of CSF and plasma sTREM2 as a potential diagnostic marker of prion disease. Our data indicate that, compared to controls, TREM2 is increased in sCJD patient brains at the mRNA and protein levels in a regional and subtype dependent fashion, and expressed in a subpopulation of microglia. In contrast, ADAM10 is increased at the protein, but not the mRNA level, with a restricted neuronal expression. Elevated CSF sTREM2 is found in sCJD, genetic CJD with mutations E200K and V210I in the prion protein gene (PRNP), and iatrogenic CJD, as compared to healthy controls (HC) (AUC = 0.78-0.90) and neurological controls (AUC = 0.73-0.85), while CSF sTREM2 is unchanged in fatal familial insomnia. sTREM2 in the CSF of cases with Alzheimer's disease, and multiple sclerosis was not significantly altered in our series. CSF sTREM2 concentrations in sCJD are PRNP codon 129 and subtype-related, correlate with CSF 14-3-3 positivity, total-tau and YKL-40, and increase with disease progression. In plasma, sTREM2 is increased in sCJD compared with HC (AUC = 0.80), displaying positive correlations with plasma total-tau, neurofilament light, and YKL-40. We conclude that comparative study of TREM2 in brain and biological fluids of prion diseases reveals TREM2 to be altered in human prion diseases with a potential value in target engagement, patient stratification, and disease monitoring.
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