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triggering-receptor
384 studies tagged triggering-receptor, dated 1986-05-01 to 2026-11-01. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
384 studies carry this tag.
Date range
1986 to 2026
Top journals
- bioRxiv 21
- Journal of neuroinflammation 17
- International journal of molecular sciences 13
- Alzheimer's & dementia : the journal of the Alzheimer's Association 10
- Glia 10
169 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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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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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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To maintain homeostasis, an organism must detect and resolve sterile tissue damage.
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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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66/100
Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease.
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In late-onset Alzheimer disease (AD) pathogenesis, genes, infections and immunity could be significant factors.
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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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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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Aging is characterized by a chronic low-grade sterile inflammation dubbed as inflammaging, which in part originates from accumulating cellular debris.
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Inflammation is a protective reaction activated in response to detrimental stimuli, such as dead cells, irritants or pathogens, by the evolutionarily conserved immune system and is regulated by the host.
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39/100
Neuroinflammation plays a prominent role in the pathogenesis of vascular dementia (VD).
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Increasing evidence suggests that changes in the triggering receptor expressed on myeloid cells 2 (TREM2) is closely correlated with the pathological development of Alzheimer's disease (AD).
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39/100
Amyloid plaques, mainly composed of abnormally aggregated amyloid β-protein (Aβ) in the brain parenchyma, and neurofibrillary tangles (NFTs), consisting of hyperphosphorylated tau protein aggregates in neurons, are two pathological hallmarks of Alzheimer's disease (AD).
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The triggering receptor expressed on myeloid cells 2 (TREM2) is a multifunctional surface protein that affects survival, migration, and phagocytic capacity of myeloid cells.
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Recent years have witnessed a revolution in our understanding of microglia biology, including their major role in the etiology and pathogenesis of neurodegenerative diseases.
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Microglial expression of PSEN2 N141I resulted in impaired γ-secretase activity as well as exaggerated inflammatory cytokine release, NFκB activity, and Aβ internalization.
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These results suggest that persons carrying certain genotypes in IL10 (-1082G/A), IL1β (1473C/G), IL6 (-174C/G), and TNFIα (-308A/G) could be more vulnerable to development of neuroinflammation, and consequently of AD.
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Microglia, the brain-resident immune cells, are critically involved in many physiological and pathological brain processes, including neurodegeneration.
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Clinically, high levels of acrolein (a highly reactive α, β-unsaturated aldehyde) and acrolein adducts are detected in the brain of patients with CNS neurodegenerative diseases, including Alzheimer's disease and spinal cord injury.
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Alzheimer's disease (AD) is the most common form of dementia characterized by the deposition of extracellular amyloid-β (Aβ)-containing plaques, the formation of intraneuronal neurofibrillary tangles as well as neuroinflammatory changes.
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Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults.
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Historically neurodegenerative diseases, Alzheimer's disease (AD) in particular, have been viewed to be primarily caused and driven by neuronal mechanisms.
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Chronic activation of brain innate immunity is a prominent feature of Alzheimer’s disease (AD) and primary tauopathies.
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45/100
Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology.
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Alzheimer's disease (AD) is the most common form of dementia in the elderly and, despite the tremendous efforts researchers have put into AD research, there are no effective options for prevention and treatment of the disease.
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Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder.
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Neurodegenerative diseases share the fact that they derive from altered proteins that undergo an unfolding process followed by formation of β-structures and a pathological tendency to self-aggregate in neuronal cells.
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Many risk genes for the development of Alzheimer's disease (AD) are exclusively or highly expressed in myeloid cells.
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The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage.
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Reactive microglia are a major pathological feature of Alzheimer's disease (AD).
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Alzheimer's disease (AD), the most common form of dementia, has emerged as a major global public health challenge.
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Microglia, being the resident immune cells of the central nervous system, play an important role in maintaining tissue homeostasis and contributes towards brain development under normal conditions.
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Astrocytes, oligodendrocytes, and microglia are abundant cell types found in the central nervous system and have been shown to play crucial roles in regulating both normal and disease states.
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Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by impairments of cognitive function as a result of synaptic deficits and neuronal loss, is associated with inflammation.
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Neuritic plaques, a pathological hallmark in Alzheimer's disease (AD) brains, comprise extracellular aggregates of amyloid-beta (Aβ) peptide and degenerating neurites that accumulate autolysosomes.
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Gene expression profiles of more than 10,000 individual microglial cells isolated from cortex and hippocampus of male and female App NL-G-F mice over time demonstrate that progressive amyloid-β accumulation accelerates two main activated microglia states that are also present during normal aging.
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The complement system plays critical roles in development, homeostasis, and regeneration in the central nervous system (CNS) throughout life; however, complement dysregulation in the CNS can lead to damage and disease.
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Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function and iron accumulation.
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The NLRP3 inflammasome is a multimeric protein complex that initiates an inflammatory form of cell death and triggers the release of proinflammatory cytokines IL-1β and IL-18.
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41/100
PLCG2 expression is restricted primarily to microglia and granule cells of the dentate gyrus.
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39/100
The accumulation of aggregated amyloid β (Aβ) peptides in the brain is deeply involved in Alzheimer disease (AD) pathogenesis.
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IL-1β, IL-18, and caspase-1 were increased whereas Aβ phagocytosis and TREM2 were reduced in LPS+Aβ42-stimulated cells.
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Alzheimer's disease (AD) is a common neurodegenerative disorder, strongly related with age.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning.
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Microglial activation is a distinguished attribute in many neurodegenerative diseases of aging.
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Microglia are resident immune cells in the central nervous system (CNS) that originate from myeloid progenitor cells in the embryonic yolk sac and are maintained independently of circulating monocytes throughout life.
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S100B is a Ca 2+ -binding protein mainly concentrated in astrocytes.
From across this tag
9 of the 384 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.
- Pyroptosis in Alzheimer's disease: cell type-specific activation in microglia, astrocytes and neurons
- Microglia in Neuroinflammation and Neurodegeneration: From Understanding to Therapy
- Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) R47H Variant Causes Distinct Age- and Sex-Dependent Musculoskeletal Alterations in Mice
- Microglia as neuroprotective, immunocompetent cells of the CNS
- Boosting angiotensin-converting enzyme (ACE) in microglia protects against Alzheimer's disease in 5xFAD mice
- Immunoproteasome Deficiency Impairs Microglial Clearance and Worsens Tau and Amyloid Pathology
- A Binding Site for CVN293 Reveals a Mechanism for Allosteric Control of THIK-1 K2P Channel Gating
- Inflammasome activation and innate immunity in Alzheimer's disease
- Simvastatin inhibits the activation of p21ras and prevents the loss of dopaminergic neurons in a mouse model of Parkinson's disease