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trem2
363 studies tagged trem2, dated 2000-05-01 to 2026-06-02. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Gain-of-function Modulation of TREM2 and its Impact on Amyloid-β and Tau Pathologies in Alzheimer's Disease: A Systematic Review and Meta-analysis of Animal Studies 2026-06-02
- The TREM2 agonistic antibody AL002 in early Alzheimer's disease: a phase 2 randomized trial 2026-03-05
- Decoding TREM2 Signaling Pathways 2026-01-09
Studies
363 studies carry this tag.
Date range
2000 to 2026
Top journals
- Molecular neurodegeneration 26
- Neurobiology of aging 16
- Neuron 10
- The Journal of experimental medicine 10
- Acta neuropathologica 9
147 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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TREM2 is an Alzheimer's disease (AD) risk gene expressed in microglia.
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Individuals with Down syndrome (DS) develop Alzheimer's disease (AD)-related neuropathology, characterized by amyloid plaques with amyloid β (Aβ) and neurofibrillary tangles with tau accumulation.
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Glia have been implicated in Alzheimer's disease (AD) pathogenesis.
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Loss-of-function (LOF) variants of TREM2, an immune receptor expressed in microglia, increase Alzheimer's disease risk.
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The present study explores the associations of soluble TREM2, an important regulator of microglial activity linked to Alzheimer's disease (AD), with other known inflammatory proteins in cerebrospinal fluid (CSF).
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Loss-of-function genetic variants of triggering receptor expressed on myeloid cells 2 (TREM2) are linked with an enhanced risk of developing dementias.
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The heterogeneous functions of dermal myeloid cells in antigen presentation, and scavenging pathogens and cell debris places them centrally in cutaneous inflammation.
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Several genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) have been shown to increase the risk of developing Alzheimer's disease (AD) supporting a role of microglia and immune cells in the pathobiology of AD.
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Adipose tissue remodeling plays a significant role in obesity-induced insulin resistance.
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Loss of function of TREM2, a key receptor selectively expressed by microglia in the brain, contributes to the development of Alzheimer's disease (AD).
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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) has been associated with Alzheimer's disease (AD).
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Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) are known to increase the risk of developing Alzheimer disease and Parkinson's disease (PD).
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Identification of multiple immune-related genetic risk factors for sporadic AD (sAD) have put the immune system center stage in mechanisms underlying this disorder.
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Stroke is the second most common cause of death and permanent disability.
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The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer's disease (AD).
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Innate immune responses are considered to play crucial roles in the progression of Alzheimer's disease (AD).
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44/100
Variants in the microglial receptor TREM2 confer risk for multiple neurodegenerative diseases.
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Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown.
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Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer's disease.
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Triggering receptor expressed in myeloid cells (TREM)2 is a genetic high-risk factor for sporadic Alzheimer's disease (AD) and is considered a potential target for AD diagnosis and therapy, although its role in the different stages of AD remains controversial.
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Microglia adopt numerous fates with homeostatic microglia (HM) and a microglial neurodegenerative phenotype (MGnD) representing two opposite ends.
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37/100
The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects.
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Variants of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased incidence of Alzheimer's disease, as well as other neurodegenerative disorders.
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Low frequency coding variants in TREM2 are associated with Alzheimer disease (AD) risk and cerebrospinal fluid (CSF) TREM2 protein levels are different between AD cases and controls.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks.
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Hair growth can be induced from resting mouse hair follicles by topical application of JAK inhibitors, suggesting that JAK-STAT signaling is required for maintaining hair follicle stem cells (HFSCs) in a quiescent state.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor genetically linked to the risk for Alzheimer's disease (AD).
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Clinically, superimposed systemic inflammation generally has significant deleterious effects on the Alzheimer's disease (AD) progression.
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Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer's disease (AD) in Caucasians.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is involved in nonmalignant pathological processes.
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Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients.
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system.
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Coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with late-onset Alzheimer's disease (AD).
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TREM2 (triggering receptor expressed on myeloid cells 2) gene variants were reported to increase the risk of Alzheimer's disease (AD) and even other neurodegenerative diseases (frontotemporal dementia (FTD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS)), but so far, no definite conclusion has been drawn.
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Alzheimer's disease (AD) is the leading cause of dementia worldwide.
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Alzheimer's disease (AD) is the leading cause of dementia.
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The microglial triggering receptor expressed on myeloid cells 2 (TREM2) signals via the activatory membrane adaptor molecule TYROBP.
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Alzheimer disease is more than a pure proteopathy.
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Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population.
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Murine microglia expressing the Alzheimer's disease-linked TREM2 R47H mutation display variable decrease in phagocytosis, while impaired phagocytosis is reported following loss of TREM2.
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CSF sTREM2 increased with systemic and CNS HIV-1 disease severity, with the highest levels found in patients with HIV-associated dementia (HAD).
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Rare coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer's disease (AD), but how they confer this risk remains uncertain.
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Alzheimer disease (AD) is a debilitating dementia believed to result from the deposition of extracellular amyloid-β (Aβ)-containing plaques followed by the formation of neurofibrillary tangles.
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TREM2 was suggested to be an important regulator of microglia during neurodegeneration, but previous studies report conflicting results in relation to soluble TREM2 (sTREM2) in cerebrospinal fluid (CSF) when using clinical criteria to classify Alzheimer's disease (AD).
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Alzheimer's disease (AD), the most common form of dementia, is characterized by the abnormal accumulation of amyloid plaques and hyperphosphorylated tau aggregates, as well as microgliosis.
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The R47H variant of the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) significantly increases the risk for late onset Alzheimer's disease.
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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is a potential and novel biomarker of neuroinflammation implicated in the onset and progression of Alzheimer's disease (AD).
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Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking.
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Microglia are activated after neuronal injury and in neurodegenerative diseases, and trigger neuroinflammation in the central nervous system (CNS).
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Dysfunction of microglia, the brain's immune cells, is linked to neurodegeneration.
From across this tag
10 of the 363 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.
- Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels
- TREM2, a DAP12-associated receptor, regulates osteoclast differentiation and function
- The innate immune response to Salmonella enterica serovar Typhimurium by macrophages is dependent on TREM2-DAP12
- Acute Trem2 reduction triggers increased microglial phagocytosis, slowing amyloid deposition in mice
- Function of TREM1 and TREM2 in Liver-Related Diseases
- Soluble TREM2 and Alzheimer-related biomarker trajectories in the blood of patients with diabetes based on their cognitive status
- Soluble TREM2: Innocent bystander or active player in neurological diseases?
- TREM2-Ligand Interactions in Health and Disease
- Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2
- Lack of genetic association between TREM2 and Alzheimer's disease in East Asian population: a systematic review and meta-analysis