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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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Alzheimer's disease (AD) is a lethal neurodegenerative disorder primarily affecting the aged population.
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Microglia are key in the homeostatic well-being of the brain and microglial dysfunction has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD).
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Variants in the triggering receptor expressed on myeloid cells 2 gene are linked with an increased risk of dementia, in particular the R47Hhet triggering receptor expressed on myeloid cells 2 variant is linked to late-onset Alzheimer's disease.
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Inflammation plays important roles in the progress of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease.
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Sepsis is a leading cause of death in critical illness, and its pathophysiology varies depending on preexisting medical conditions.
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Triggering receptor expressed on myeloid cells 2 (TREM2) has been suggested to play a crucial role in Alzheimer's disease (AD) pathogenesis, as revealed by genome-wide association studies (GWAS).
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Microglia, resident immune cells of the central nervous system (CNS), play a pivotal role in immune surveillance and maintenance of neuronal health.
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Ageing is characterized by the development of persistent pro-inflammatory responses that contribute to atherosclerosis, metabolic syndrome, cancer and frailty 1-3 .
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Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau.
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By engaging membrane-bound TREM2, the selected antibody was shown to promote their cellular proliferation, uptake of oligomeric beta amyloid/apoptotic neurons, and activation in a Syk and Akt dependent manner.
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The innate immune system plays key roles in controlling Alzheimer's disease (AD), while secreting cytokines to eliminate pathogens and regulating brain homeostasis.
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Alzheimer's Disease (AD) is the most prevalent form of dementia across the world.
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Alzheimer's disease (AD) is the main cause of dementia worldwide.
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Alzheimer's disease (AD) is the most prevalent neurodegenerative disease commonly diagnosed among the elderly population.
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Triggering receptor expressed on myeloid cells 2 (TREM2) sustains microglia response to brain injury stimuli including apoptotic cells, myelin damage, and amyloid β (Aβ).
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Alzheimer's disease (AD) is the most common form of dementia.
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TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response.
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Periodontitis is the sixth most prevalent diseases around the globe, which is closely related to many systemic diseases and affects general health.
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Cerebrovascular pathologies occur in up to 80% of cases of Alzheimer's disease; however, the underlying mechanisms that lead to perivascular pathology and accompanying blood-brain barrier (BBB) disruption are still not fully understood.
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The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor expressed on myeloid-derived cell types.
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Herein, we demonstrate that endogenous Tyrobp transcription is specifically increased in recruited microglia.
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TREM1 and TREM2 are members of the triggering receptors expressed on myeloid cells (TREM) family.
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Neuroinflammation is associated with neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis.
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Locus Coeruleus (LC) is the main noradrenergic nucleus of the central nervous system, and its neurons widely innervate the whole brain.
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TREM2 is a microglial cell surface receptor, with risk mutations linked to Alzheimer's disease (AD), including R47H. TREM2 signalling via SYK aids phagocytosis, chemotaxis, survival, and changes to microglial activation state.
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To maintain homeostasis, an organism must detect and resolve sterile tissue damage.
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Triggering receptor expressed on myeloid cells 2 (TREM2), a receptor exclusively expressed by microglia in the brain, modulates microglial immune homeostasis.
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Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer's disease (AD).
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Alogliptin treatment alleviated LPS-induced cognitive impairment as assessed by Morris water maze and novel object recognition tests.
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The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology.
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66/100
Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease.
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The discovery of TREM2 as a myeloid-specific Alzheimer's disease (AD) risk gene has accelerated research into the role of microglia in AD.
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Triggering receptor expressed on myeloid cells 2 (TREM2) has been shown with a neuroprotective function against inflammation and neuronal injury in Alzheimer's disease (AD).
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Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD).
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52/100
Identifying factors underlying resistance to immune checkpoint therapy (ICT) is still challenging.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is an immune receptor expressed on microglia that also can become soluble (sTREM2).
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The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD).
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In late-onset Alzheimer disease (AD) pathogenesis, genes, infections and immunity could be significant factors.
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TREM2 is a receptor for lipids expressed in microglia.
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Alzheimer's disease (AD) is characterized by plaques containing amyloid-β (Aβ) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau.
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Beta-amyloid deposition is a defining feature of Alzheimer's disease (AD).
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Triggering receptor expressed on myeloid cell-2 (TREM2) is a lipid and lipoprotein binding receptor expressed by cells of myeloid origin.
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Neurodegenerative disorders, such as Alzheimer's disease, are a global public health burden with poorly understood aetiology.
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Cell function and activity are regulated through integration of signaling, epigenetic, transcriptional, and metabolic pathways.
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Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells.
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Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms.
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Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid.
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Neurodegenerative diseases are neuronal disorders characterized by the loss of a large number of neurons in the human brain.
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39/100
Alzheimer's disease is characterized by aggregated amyloid beta plaques and neurofibrillary tangles.
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44/100
Alzheimer's Disease (AD) is a neurodegenerative disorder influenced by aging and genetic risk factors.
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.
- Cerebrospinal Fluid Markers of Alzheimer's Disease Pathology and Microglial Activation are Associated with Altered White Matter Microstructure in Asymptomatic Adults at Risk for Alzheimer's Disease
- TREM2 inhibition triggers antitumor cell activity of myeloid cells in glioblastoma
- TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity
- Imbalance of Microglial TLR4/TREM2 in LPS-Treated APP/PS1 Transgenic Mice: A Potential Link Between Alzheimer's Disease and Systemic Inflammation
- Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients
- Electroacupuncture alleviate cognitive impairment via activation of TREM2-positive microglia in APP/PS1 mice
- Role of neuroinflammation in neurodegeneration development
- Cannabinoid CB2Receptors and Fatty Acid Amide Hydrolase Are Selectively Overexpressed in Neuritic Plaque-Associated Glia in Alzheimer's Disease Brains
- Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) positively regulates lipopolysaccharide-induced expression of CXC chemokine ligand 10 and 11 in mouse macrophages
- The FTD-like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism