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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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41/100
Alzheimer's disease (AD), also known as senile dementia, is the most common degenerative disease of the central nervous system.
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Microglia, the macrophages of the brain, are vital for brain homeostasis and have been implicated in a broad range of brain disorders.
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Recent studies showed increased expression of complements in various neurodegenerative diseases, including Alzheimer's and Parkinson's diseases.
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Mutations in a microglia-associated gene TREM2 increase the risk of Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays important roles in brain microglial function in neurodegenerative diseases, but the role of TREM2 in the GBM TME has not been examined.
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Alzheimer's Disease is the most common form of dementia; its key pathological findings include the deposition of extracellular-neurotoxic-plaques composed of amyloid-beta (Ab).
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CUMS induced depressive-like behaviors and cognitive decline in mice, which could be reversed by inhibiting NLRP3 inflammasome.
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Disordered lipid accumulation in the arterial wall is a hallmark of atherosclerosis.
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TREM2 is an innate immune receptor expressed by microglia in the adult brain.
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Sleep loss is associated with cognitive decline in the aging population and is a risk factor for Alzheimer's disease (AD).
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Natural killer (NK) cells are commonly reduced in human tumors, enabling many to evade surveillance.
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Previously, we reported that H157Y, a rare coding variant on exon 3 of the triggering receptor expressed on myeloid cells 2 gene (TREM2), was associated with Alzheimer's disease (AD) risk in a Han Chinese population.
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43/100
Idiopathic pulmonary fibrosis (IPF) is a lung disease with high mortality, limited treatment options and an unknown aetiology.
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During the 4-day meeting, presenters illuminated aspects of the cross-talk between APOE and immunity, with a focus on the roles of microglia, triggering receptor expressed on myeloid cells 2 (TREM2), and components of inflammation (e.g., tumor necrosis factor α [TNFα]).
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TREM2 is a myeloid cell receptor that has been extensively described in the context of neuroinflammation and neurodegenerative diseases.
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Alzheimer's disease (AD) is associated with the cerebral deposition of Amyloid-β (Aβ) peptide, which leads to NLRP3 inflammasome activation and subsequent release of interleukin-1β (IL-1β) and interleukin-18 (IL-18).
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60/100
Loss of nuclear TDP-43 is a hallmark of neurodegeneration in TDP-43 proteinopathies, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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In activated microglia, cholesterol enrichment promoted the release of encapsulated IL-1β accompanied by a switch to a more neuroprotective phenotype, with increased phagocytic capacity and release of neurotrophic factors.
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& aims The immune landscape of hepatocellular carcinoma (HCC) following transarterial chemoembolisation (TACE) remains to be clarified.
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β2-Microglobulin (β2M), a component of the major histocompatibility complex class I molecule, is associated with aging-related cognitive impairment and Alzheimer's disease.
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Microglia and neuroinflammation are implicated in the development and progression of Alzheimer's disease (AD).
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The repair of white matter injury is of significant importance for functional recovery after ischemic stroke, and the up-regulation of triggering receptors expressed on myeloid cells 2 (TREM2) after ischemic stroke is neuroprotective and implicated in remyelination.
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Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mutant allele that produces a confounding reduction in protein product.
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Translocase of outer mitochondrial membrane 40 (TOMM40) is located in the outer membrane of mitochondria.
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Expansion of the hexanucleotide repeat GGGGCC in the C9orf72 gene is the most common genetic factor in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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The complement system is an ancient collection of proteolytic cascades with well-described roles in regulation of innate and adaptive immunity.
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Alzheimer's disease (AD) is characterized by synaptic loss, which can result from dysfunctional microglial phagocytosis and complement activation.
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Consistent with previous in vitro findings, Trem2 H157Y increases TREM2 shedding with elevated soluble TREM2 levels in the brain and serum.
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Triggering receptor expressed on myeloid cells-2 (TREM2), a cell surface receptor mainly expressed on microglia, has been shown to play a critical role in Alzheimer's disease (AD) pathogenesis and progression.
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Nonalcoholic fatty liver disease (NAFLD) is the most common liver pathology worldwide.
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Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD), suggesting that activation of this innate immune receptor may be a useful therapeutic strategy.
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48/100
Sepsis-induced cardiomyopathy (SICM) is common in septic patients with a high mortality and is characterized by an abnormal immune response.
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Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression.
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Current hypothesis of Alzheimer's disease (AD) postulates that amyloid β (Aβ) deposition in the brain causes tau inclusion in neurons and leads to cognitive decline.
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Microglia are central players in brain innate immunity and have been the subject of extensive research in Alzheimer's disease (AD).
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52/100
BACKGROUNDSoluble triggering receptor expressed on myeloid cells 2 (sTREM2) plays an important role in the clearance of pathological amyloid-β (Aβ) in Alzheimer's disease (AD).
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Obesity-induced chronic liver inflammation is a hallmark of nonalcoholic steatohepatitis (NASH)-an aggressive form of nonalcoholic fatty liver disease.
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The major neuropathological hallmarks of Alzheimer's disease (AD) are amyloid β (Aβ) plaques and neurofibrillary tangles (NFT), accompanied by neuroinflammation and neuronal loss.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is a key pro-tumorigenic marker of tumor-infiltrating macrophages, showing potent immunosuppressive activity in tumor microenvironment.
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The rs75932628 was associated with AD in the Greek sample.
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Neuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI).
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Adult neurogenesis occurs mainly in the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles.
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53/100
In addition to tau and Aβ pathologies, inflammation plays an important role in Alzheimer's disease (AD).
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Brain iron accumulation, which is indicated in the cerebrospinal fluid (CSF) ferritin, is associated with the development of Alzheimer's Disease (AD).
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47/100
Using spatial cell-type-enriched transcriptomics, we compare plaque-induced gene (PIG) expression in microglia-touching plaques, neighboring plaques, and far from plaques in an aged Alzheimer's mouse model with late plaque development.
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Synapses are bridges for information transmission in the central nervous system (CNS), and synaptic plasticity is fundamental for the normal function of synapses, contributing substantially to learning and memory.
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Traumatic brain injury (TBI) promotes several Alzheimer's disease-like pathological features, including microtubule-associated protein tau (MAPT) accumulation within neurons.
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The expression of the triggering receptor on myeloid cell-2 (TREM2) knockdown in microglia from the lateral habenula (LHb) reportedly induces depression-like behaviors in mice.
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There is a huge need for novel therapeutic and preventative approaches to Alzheimer's disease (AD) and neuroinflammation seems to be one of the most fascinating solutions.
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Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer's disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy economic burden on families and society.
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.
- Secretases in Alzheimer's disease: Novel insights into proteolysis of APP and TREM2
- TREM2 promotes Aβ phagocytosis by upregulating C/EBPα-dependent CD36 expression in microglia
- Beta-amyloid-stimulated microglia induce neuron death via synergistic stimulation of tumor necrosis factor alpha and NMDA receptors
- Microglial mTOR Activation Upregulates Trem2 and Enhances β-Amyloid Plaque Clearance in the 5XFAD Alzheimer's Disease Model
- Impact of TREM2R47H variant on tau pathology-induced gliosis and neurodegeneration
- The therapeutic potential of TREM2 in cancer
- Overexpression of TREM2 enhances glioma cell proliferation and invasion: a therapeutic target in human glioma
- TREM2 variants and risk of Alzheimer's disease: a meta-analysis
- Interaction between genetic factors, Porphyromonas gingivalis and microglia to promote Alzheimer's disease
- NLRP3 inflammasome activation and cell death