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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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Glioblastomas (GBM) are incurable central nervous system (CNS) cancers characterized by substantial myeloid cell infiltration.
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CSF sTREM2 levels are positively associated with an increased risk of AD and MCI.
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Microglia are a specialized type of neuroimmune cells that undergo morphological and molecular changes through multiple signaling pathways in response to pathological protein aggregates, neuronal death, tissue injury, or infections.
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The gut microbiota and tumor-associated macrophages (TAMs) affect tumor responses to anti-programmed cell death protein 1 (PD-1) immune checkpoint blockade.
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54/100
Morphologically, reactive and amoeboid microglia were common in mixed DLB + AD, while homeostatic microglia with a small soma and thin processes were observed in pure DLB cases.
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47/100
Trem2 (triggering receptor on myeloid cells 2), a surface lipid receptor, is expressed on foamy macrophages within atherosclerotic lesions and regulates cell survival, proliferation, and anti-inflammatory responses.
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We proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model.
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Alzheimer's disease (AD) and dementia in general are age-related diseases with multiple contributing factors, including brain inflammation.
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Frontotemporal dementia (FTD) is an incurable group of early-onset dementias that can be caused by the deposition of hyperphosphorylated tau in patient brains.
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Microglia play a pivotal role in the pathology of Alzheimer's Disease (AD), with the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) central to their neuroprotective functions.
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46/100
High levels of proinflammatory cytokines induce neurotoxicity and catalyze inflammation-driven neurodegeneration, but the specific release mechanisms from microglia remain elusive.
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Chronic periodontitis and its keystone pathogen, Porphyromonas gingivalis, have increasingly been linked with Alzheimer's disease (AD).
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Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH), is an advanced stage of metabolic fatty liver disease.
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Atherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in the intimal layer of arteries, and its main complications, myocardial infarction and stroke, are the leading cause of mortality worldwide [1], [2].
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Osteoarthritis (OA) is the most prominent chronic arthritic disease, affecting over 3 billion people globally.
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43/100
ITM2B/BRI2 mutations cause Alzheimer's Disease (AD)-related dementias.
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Outer retinal degenerations, including age-related macular degeneration (AMD), are characterized by photoreceptor and retinal pigment epithelium (RPE) atrophy.
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43/100
Triggering receptor expressed on myeloid cells 2 (TREM2) is a membrane glycoprotein that plays a crucial role in the regulation of microglial survival, activation, phagocytosis, as well as in the maintenance of brain homeostasis and the inflammatory response to injury or neurodegeneration.
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Aducanumab, an anti-amyloid immunotherapy for Alzheimer's disease, efficiently reduces Aβ, though its plaque clearance mechanisms, long-term effects, and effects of discontinuation are not fully understood.
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45/100
This molecular genetics study found that several TREM2 gene variants previously thought to work only by altering the TREM2 protein itself, also disrupt how the TREM2 gene's RNA message is spliced together, sometimes producing dysfunctional protein versions.
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Efferocytosis and metabolic reprogramming of macrophages play crucial roles in myocardial infarction (MI) repair.
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis.
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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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Triggering receptor expressed on myeloid cells 2 (TREM2) is upregulated in activated microglia and may be related to cognitive decline in patients with Alzheimer's disease (AD).
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Alzheimer's disease is a pervasive neurodegenerative disease that is estimated to represent approximately 70% of dementia cases worldwide, and the molecular complexity that has been highlighted remains poorly understood.
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Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in brain microglia, with variants that are associated with neurodegenerative diseases, including Alzheimer's disease.
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Microglial cells are well known to be implicated in the pathogenesis of Alzheimer's disease (AD), due to the impaired clearance of amyloid-β (Aβ) protein.
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Cancer mortality primarily stems from metastatic recurrence, emphasizing the urgent need for developing effective metastasis-targeted immunotherapies.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane receptor protein predominantly expressed in microglia within the central nervous system (CNS).
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Microglia and neuroinflammation play an important role in the development and progression of Alzheimer's disease (AD).
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43/100
In vitro, PCSK9 significantly increased IL6, IL1B and TNFΑ mRNA levels in Aβ fibrils-treated U373 cells, without influencing inflammasome gene expression, except for an increase in NLRC4 mRNA levels.
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47/100
Multiple sclerosis remains one of the most common causes of neurological disability in the young adult population (aged 18-40 years).
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Neuroinflammation is an inflammatory cascade involved in various neurological disorders, including Alzheimer's disease, multiple sclerosis, and other relevant diseases.
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Microglia-mediated neuroinflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD).
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Neurodegenerative disorders, including Alzheimer's disease, are associated with microgliosis.
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Alzheimer's disease (AD) is ranked as the third-most expensive illness and sixth leading cause of mortality.
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Atherosclerosis is driven by the expansion of cholesterol-loaded 'foamy' macrophages in the arterial intima.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein that is predominantly expressed by microglia in the brain.
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The aim of this review is to explore the role of NLRP3 activation-mediated neuronal pyroptosis and neuroinflammation in neurodegenerative diseases.
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Alzheimer's disease (AD) is the most prevalent cause of dementia worldwide.
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Neuroinflammation is a key pathological feature in neurological diseases, including Alzheimer's disease (AD).
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Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood.
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Amyloid plaques are considered to be the pathological hallmark of Alzheimer's disease (AD).
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Neuronal hyperactivity is a key feature of early stages of Alzheimer's disease (AD).
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Chimeric antigen receptor (CAR) -T cell therapy is an efficient therapeutic strategy for specific hematologic malignancies.
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51/100
Alzheimer's disease (AD) remains one of the grand challenges facing human society.
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Alzheimer's disease (AD) is the most common neurodegenerative disease, resulting in the loss of cognitive ability and memory.
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Colony-stimulating factor-1 receptor (CSF-1R)-related leukoencephalopathy (CRL) is a neurodegenerative disease that triggers early demyelination, leading to an adult-onset dementia.
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Studies in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Amyotrophic lateral sclerosis, Huntington's disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is strongly linked to Alzheimer's disease (AD) risk, but its functions are not fully understood.
From across this tag
9 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 9. The same 9 appear here every time.
- TREM2 Overexpression has No Improvement on Neuropathology and Cognitive Impairment in Aging APPswe/PS1dE9 Mice
- TREM2 Binds to Apolipoproteins, Including APOE and CLU/APOJ, and Thereby Facilitates Uptake of Amyloid-Beta by Microglia
- Efficient colonic mucosal wound repair requires Trem2 signaling
- Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) R47H Variant Causes Distinct Age- and Sex-Dependent Musculoskeletal Alterations in Mice
- PLCG2 protective variant p.P522R modulates tau pathology and disease progression in patients with mild cognitive impairment
- The surface-exposed chaperone, Hsp60, is an agonist of the microglial TREM2 receptor
- Soluble α-synuclein-antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia
- Donepezil Regulates LPS and Aβ-Stimulated Neuroinflammation through MAPK/NLRP3 Inflammasome/STAT3 Signaling
- Pathological Roles of INPP5D in Alzheimer's Disease