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myeloid
747 studies tagged myeloid, dated 1986-05-01 to 2026-11-01. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
747 studies carry this tag.
Date range
1986 to 2026
Top journals
- Molecular neurodegeneration 31
- Journal of neuroinflammation 26
- bioRxiv 21
- Alzheimer's & dementia : the journal of the Alzheimer's Association 19
- Neurobiology of aging 19
252 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation.
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There is significant evidence that microglia contribute to neuroinflammation and neurotoxicity in AD 1,2 , yet there is also evidence to the contrary.
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43/100
Neuroinflammation plays a vital role in determining the trajectory of Alzheimer's disease (AD) progression.
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Peruvian GWAS identified Amerindian ancestry specific exonic AD susceptibility variant p.H157Y. This variant has been previously reported as AD marker in Han Chinese populations with extreme effect size, but its rarity and contradictory findings in other groups suggest a potential ancestry‐specific effect.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor abundantly expressed in microglia in the brain.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is cell surface transmembrane receptor of the TREM family, predominantly expressed on microglia within the central nervous system (CNS).
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Alcohol use disorders (AUDs) affect substantial populations worldwide and increase the risk of developing cognitive impairments and alcohol-associated dementia.
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ACAT1 inhibition increased LRP1 levels and soluble TREM2 (sTREM2) release via enhanced TREM2 cleavage by ADAM metallopeptidase domain 10/17 (ADAM10/17).
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Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been demonstrated to increase the risk of late-onset Alzheimer's disease (AD) and Nasu-Hakola disease.
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In the MWM, syringin reduced escape latency.
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We previously reported that T96K is a gain-of-function mutation in TREM2 based on its ability to increase ligand-dependent activation.
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Inflammation is a key factor in neurodegenerative diseases (NDs) development, such as Alzheimer's disease (AD) and Parkinson's disease (PD).
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Protective PLCG2P522R microglia showed significant transcriptomic similarity to isogenic controls.
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Chronic neuroinflammation and impaired protein clearance are hallmarks of neurodegenerative diseases such as Alzheimer's disease (AD) and HIV-associated neurocognitive disorders (HAND).
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Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), represent significant global health challenges, affecting millions and straining healthcare systems.
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We identified a significant upregulation of COX-1 in 5 × FAD mice, with expression specifically localized to microglia in an age-dependent manner.
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The amyloid/tau/neurodegeneration (ATN) biomarker framework has greatly progressed the diagnosis and staging of Alzheimer's disease (AD).
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Ms4a4a deficiency reduced steady-state Aβ levels and shortened its half-life in brain interstitial fluid.
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Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD).
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Genome-wide association studies have identified many gene polymorphisms associated with an increased risk of developing late-onset Alzheimer's disease (LOAD).
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Our results demonstrate CA effectively inhibits NLRP3 inflammasome activation, reduces microglial pyroptosis, and mitigates oxidative stress-induced mitochondrial impairment in BV-2 cells.
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M07-TFN showed higher binding affinities and stronger activation of hTREM2 signaling than all previously described anti-hTREM2 antibodies. p-Syk activation was increased 30-fold in hTREM2-overexpressing HEK293 cells and fourfold in human microglia cells compared to baseline.
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Alzheimer's disease (AD) is a typical neurodegenerative disease, with the most highlighted pathologic changes identified in the β-amyloid peptide (Aβ) and neurofibrillary tangles (NFTs).
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43/100
Alzheimer's disease (AD) and age-related macular degeneration (AMD) represent the leading causes of dementia and vision impairment in the elderly, respectively.
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Neurodegenerative diseases, including Alzheimer's and Parkinson's disease, affect an increasing number of people in aging societies, dramatically reducing the quality of life of those affected.
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In 5xFAD mice, the absence of PLCG2 resulted in reduced TREM2 expression and impaired microglial associations with amyloid beta plaques.
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Growing genetic and pathological evidence has identified microglial dysfunction as a key contributor to the pathogenesis and progression of various neurological disorders, positioning microglia replacement as a promising therapeutic strategy.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor predominantly expressed by microglia in the brain.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available.
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We found that pharmacological activation of TREM2 suppressed laser-induced choroidal neovessel formation.
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TREM2, a microglia-specific receptor, is strongly associated with Alzheimer's disease (AD) risk, mediating microglial responses to amyloid pathology critical to AD development.
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Neuroinflammation plays an important role in the pathogenesis of various central nervous system (CNS) diseases.
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54/100
Lung macrophages play a pivotal role in pulmonary fibrosis, with monocyte-derived alveolar macrophages driving disease progression.
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43/100
Microglia impact brain development, homeostasis, and pathology.
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Dysregulated microglia activation, leading to neuroinflammation, is crucial in neurodegenerative disease development and progression.
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Neuraminidase 1 (NEU1) cleaves terminal sialic acids from sialoglycoproteins in endolysosomes and at the plasma membrane.
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Variants of the gene triggering receptor expressed on myeloid cells-2 (TREM2) increase the risk of Alzheimer's disease (AD) and other neurodegenerative disorders.
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EQW affected FCN2 (Cohen's d -0.019), PAI-1 (Cohen's d -0.033), sVCAM-1 (Cohen's d 0.035) and a cytokine-cytokine cluster (Cohen's d 0.037) significantly compared with placebo.
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The 64Cu-labeled antibodies were obtained in high radiochemical purity (RCP), radiochemical yield (RCY), and specific activity.
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In the central nervous system, triggering receptor expressed on myeloid cells 2 (TREM2) is exclusively expressed by microglia and is critical for microglial proliferation, migration, and phagocytosis.
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The pathological role of interferon signaling is emerging in neuroinflammatory disorders, yet, the specific role of Interferon Regulatory Factor 3 (IRF3) in neuroinflammation remains poorly understood.
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There is an urgent need for effective disease-modifying therapeutic interventions for Alzheimer's disease (AD)-the most prevalent cause of dementia with a profound socioeconomic burden.
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54/100
While macrophage heterogeneity during metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood.
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Frontotemporal dementia and amyotrophic lateral sclerosis are neurodegenerative diseases with considerable clinical, genetic and pathological overlap.
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We report CSF soluble TREM2 (sTREM2) and CSF chitinase-3-like protein 1 (CHI3L1/YKL-40) as PD biomarkers for the TREM2 agonist hPara.09.
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TREM2 trimers remained stably bound, driven primarily by salt bridge between residues D87 and R76 at the interface of TREM2 units.
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43/100
Microglia, as resident macrophages in the central nervous system, play a multifunctional role in the pathogenesis of Alzheimer's disease (AD).
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This review substantiates the evolving understanding of TREM2's disease progression-dependent impacts.
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The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor that affects cellular phenotypes by modulating phagocytosis and metabolism, promoting cell survival, and counteracting inflammation.
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Our results showed that IHT ameliorated cognitive function and Aβ pathology.
From across this tag
10 of the 747 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Microglial response to amyloid plaques in APPsw transgenic mice
- Transcriptome landscape of myeloid cells in human skin reveals diversity, rare populations and putative DC progenitors
- TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice
- R47H Variant of TREM2 Associated With Alzheimer Disease in a Large Late-Onset Family: Clinical, Genetic, and Neuropathological Study
- Eliminating microglia in Alzheimer's mice prevents neuronal loss without modulating amyloid-β pathology
- Cellular and molecular influencers of neuroinflammation in Alzheimer's disease: Recent concepts & roles
- TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson's disease
- Activation of microglial cells by beta-amyloid protein and interferon-gamma
- Microglia-mediated neuroinflammation in neurodegenerative diseases
- Spatiotemporal dynamics of macrophage heterogeneity and a potential function of Trem2hi macrophages in infarcted hearts