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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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Activation of glial cells and neuroinflammation play an important role in the onset and development of Alzheimer's disease (AD).
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Approximately ten million people are diagnosed with dementia annually since they experience difficulties with memory and thinking skills.
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Alzheimer's disease is a type of dementia characterized by problems with short-term memory, cognition, and difficulties with activities of daily living.
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Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease.
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Physical exercise is generally beneficial to all aspects of human and animal health, slowing cognitive ageing and neurodegeneration 1 .
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Alzheimer's disease (AD) is a form of dementia characterized by progressive memory decline and cognitive dysfunction.
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53/100
The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( TREM2 ), a microglia-specific gene in the brain, increases risk for late-onset Alzheimer’s disease (AD).
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Non-neuronal responses in neurodegenerative disease have received increasing attention as important contributors to disease pathogenesis and progression.
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Skin allo- and xenotransplantation are the standard treatment for major burns when donor sites for autografts are not available.
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Secretases are a group of proteases that are major drug targets considered for the prevention and treatment of Alzheimer's disease (AD).
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The mechanism of sphingosine-1-phosphate (S1P)-mediated phagocytosis remains unknown.
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Recent studies indicate that the adaptive immune system plays a role in Lewy body dementia (LBD).
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Alzheimer's disease (AD), an extremely common neurodegenerative disorder of the older generation, is one of the leading causes of death globally.
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50/100
Late-onset Alzheimer's disease (AD; LOAD) is the most common human neurodegenerative disease, however, the availability and efficacy of disease-modifying interventions is severely lacking.
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Converting checkpoint inhibitor (CPI)-resistant individuals to being responsive requires identifying suppressive mechanisms.
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The acetylcholinesterase inhibitors donepezil and rivastigmine have been used as therapeutic drugs for Alzheimer's disease (AD), but their effects on LPS- and Aβ-induced neuroinflammatory responses and the underlying molecular pathways have not been studied in detail in vitro and in vivo.
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Loss-of-function variants of triggering receptor expressed on myeloid cells 2 (TREM2) increase the risk of developing Alzheimer's disease (AD).
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Microglia are the resident macrophages of the central nervous system (CNS) acting as the first line of defense in the brain by phagocytosing harmful pathogens and cellular debris.
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As resident immune cells of the brain, microglia serve pivotal roles in regulating neuronal function under both physiological and pathological conditions, including aging and the most prevalent neurodegenerative disease, Alzheimer's disease (AD).
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Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic.
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Rare coding variants of the microglial triggering receptor expressed on myeloid cells 2 (TREM2) confer an increased risk for Alzheimer's disease (AD) characterized by the progressive accumulation of aggregated forms of amyloid β peptides (Aβ).
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Upon demyelinating injury, microglia orchestrate a regenerative response that promotes myelin repair, thereby restoring rapid signal propagation and protecting axons from further damage.
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41/100
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease.
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41/100
Alzheimer's disease (AD) is a neurodegenerative disorder with no clear causative event making the disease difficult to diagnose and treat.
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The NLRP3 inflammasome is a cytosolic multiprotein complex composed of the innate immune receptor protein NLRP3, adapter protein ASC, and inflammatory protease caspase-1 that responds to microbial infection, endogenous danger signals, and environmental stimuli.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by an increasing deterioration of memory, which is concomitant with additional cognitive deficits.
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The autophagy-lysosomal pathway plays a critical role in intracellular clearance and metabolic homeostasis.
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47/100
Heterozygous genetic variants within the TREM2 gene show a strong association with increased Alzheimer's disease (AD) risk.
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Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer's disease (AD), which results in memory impairment.
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Clinical trials of new drugs for Alzheimer's disease (AD) have ended with disappointing results, with tremendous resources and time.
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Immune surveillance is an essential process that safeguards the homeostasis of a healthy brain.
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Neuroinflammation contributes to Alzheimer's disease (AD) progression.
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The role of microglia cells in Alzheimer's disease (AD) is well recognized, however their molecular and functional diversity remain unclear.
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Here, we demonstrated for the first time that CD3-CD122+NK1.1+ precursor NK (pNK) cells expressed TREM2 and their population increased in TREM2-overexpressing transgenic (TREM2-TG) mice compared with that in female C57BL/6 J wild type (WT) mice.
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41/100
Neurodegeneration is a debilitating condition that causes nerve cell degeneration or death.
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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.
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Mycobacterial cell-wall glycolipids elicit an anti-mycobacterial immune response via FcRγ-associated C-type lectin receptors, including Mincle, and caspase-recruitment domain family member 9 (CARD9).
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41/100
Parkinson's disease is characterized by accumulation of α-synuclein (αSyn).
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The central role of the resident innate immune cells of the brain (microglia) in neurodegeneration has become clear over the past few years largely through genome-wide association studies (GWAS), and has rapidly become an active area of research.
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Triggering receptor expressed on myeloid cells-2 (TREM2) and colony-stimulating factor 1 receptor (CSF1R) are crucial molecules for microgliopathy, which is characterized by microglia dysfunction and has recently been proposed as the neuropathological hallmark of neurological disorders.
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The innate immune system is a viable target for therapeutic intervention in AD.
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There is growing evidence that excessive microglial phagocytosis of neurons and synapses contributes to multiple brain pathologies.
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The prevalence of neurodegenerative disease has increased significantly in recent years, and with a rapidly aging global population, this trend is expected to continue.
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Microglia performs a variety of functions during brain development designed to maintain brain homeostasis.
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51/100
Loss-of-function TREM2 mutations strongly increase Alzheimer's disease (AD) risk.
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The primary cohort included 91 AAs and 868 NHWs.
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Excessive microglial activation might be a central pathological process in GRN-related frontotemporal dementia (FTD-GRN).
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The complement system is part of the innate immune system that comprises several small proteins activated by sequential cleavages.
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49/100
Obesity-induced white adipose tissue (WAT) hypertrophy is associated with elevated adipose tissue macrophage (ATM) content.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity.
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.
- Decoding Mast Cell-Microglia Communication in Neurodegenerative Diseases
- Triggering receptor expressed on myeloid cells 2 (TREM2) dependent microglial activation promotes cisplatin-induced peripheral neuropathy in mice
- Gene expression and functional deficits underlie TREM2-knockout microglia responses in human models of Alzheimer's disease
- A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia
- Stavudine Reduces NLRP3 Inflammasome Activation and Modulates Amyloid-β Autophagy
- TREM2 Inhibits Tau Hyperphosphorylation and Neuronal Apoptosis via the PI3K/Akt/GSK-3β Signaling Pathway In vivo and In vitro
- Trem2 Enhances Demyelination in the Csf1r+/- Mouse Model of Leukoencephalopathy
- The triggering receptor expressed on myeloid cells 2: "TREM-ming" the inflammatory component associated with Alzheimer's disease
- iPSC-Derived Human Microglia-like Cells to Study Neurological Diseases
- New insights on the role of microglia in synaptic pruning in health and disease