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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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Macrophage recognition of Salmonella enterica serovar Typhimurium leads to a cascade of signaling events, including the activation of Src family and Syk kinases and the production of reactive oxygen species (ROS), which are critical for host innate defense during early stages of bacterial infection.
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In multiple sclerosis, inflammation can successfully be prevented, while promoting repair is still a major challenge.
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36/100
Photoreceptor apoptosis is a major cause of visual loss in retinal detachment (RD) and several other visual disorders, but the underlying mechanisms remain elusive.
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While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease.
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Microglial activation similar to that which occurs in peripheral macrophages during inflammatory attack was first demonstrated in the Alzheimer's disease (AD) brain two decades ago.
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Central nervous system (CNS) immune privilege is an experimentally defined phenomenon.
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The triggering receptor expressed on myeloid cells 2 (TREM-2) delivers intracellular signals through the adaptor DAP12 to regulate myeloid cell function both within and outside the immune system.
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DAP12 is an ITAM-containing adapter that associates with receptors in myeloid and NK cells.
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38/100
Here we showed that activation of primary astrocytes from TR APOE mice with LPS led to TR APOE-dependent differences in cytokine secretion that were greatest in TR APOE2 and that were associated with differences in NF-kappaB subunit activity.
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For many years, the central nervous system (CNS) was considered to be 'immune privileged', neither susceptible to nor contributing to inflammation.
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In Alzheimer's disease (AD) there is increasing evidence that neurotoxicity is mediated by CNS inflammatory processes.
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These results provide new evidence that TREM2 regulates OC function independent of its effects on multinucleated OC differentiation.
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The contribution of inflammation to the progression of neurodegenerative diseases such as Alzheimer's, Parkinson's, and prion diseases is poorly understood.
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Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD).
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Although abundant reactive microglia are found associated with beta-amyloid (Abeta) plaques in Alzheimer's disease (AD) brains, their contribution to cell loss remains speculative.
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Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts.
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Alzheimer's disease (AD) is characterized by enhanced beta-amyloid peptide (betaA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits.
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36/100
Triggering members of the DR family by death ligands results in the transduction of either apoptotic or survival signals.
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Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells.
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Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes.
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Caspases mediate essential key proteolytic events in inflammatory cascades and the apoptotic cell death pathway.
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The endocannabinoid system is still poorly understood.
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52/100
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), Nasu-Hakola disease, is a globally distributed recessively inherited disease.
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We recently described the cloning of murine triggering receptor expressed by myeloid cells (TREM) 2, a single Ig domain DNAX adaptor protein 12-associated receptor expressed by cells of the myeloid lineage.
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Triggering receptors expressed by myeloid cells (TREMs) belong to a rapidly expanding family of receptors that include activating and inhibitory isoforms encoded by a gene cluster linked to the MHC.
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We have characterized a cluster of single immunoglobulin variable (IgV) domain receptors centromeric of the major histocompatibility complex (MHC) on human chromosome 6.
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Evidence from postmortem analysis implicates the involvement of microglia in the neurodegenerative process of several degenerative neurological diseases, including Alzheimer's disease and Parkinson's disease.
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Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury.
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The role of glial cells is to support and sustain proper neuronal function and microglia are no exception to this.
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Scavenger receptor class A (SR-A, CD204), scavenger receptor-BI (SR-BI), and CD36 are cell surface proteins that mediate cell adhesion to, and endocytosis of, various native and pathologically modified substances, and participate in intracellular signaling, lipid metabolism, and host defense against bacterial pathogens.
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Reactive microglia associated with the beta-amyloid plaques in Alzheimer's disease (AD) brains initiate a sequence of inflammatory events integral to the disease process.
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The cytokine interleukin 1 (IL-1) has diverse actions in the brain.
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36/100
The brain in Alzheimer's disease (AD) shows a chronic inflammatory response characterized by activated glial cells and increased expression of cytokines and complement factors surrounding amyloid deposits.
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We have identified new activating receptors of the Ig superfamily expressed on human myeloid cells, called TREM (triggering receptor expressed on myeloid cells).
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It is now generally accepted that the lesions of Alzheimer disease (AD) are associated with a host of inflammatory molecules, including complement proteins, as well as with many activated microglia.
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Microglia are the principal immune cells in the central nervous system (CNS) and have a critical role in host defense against invading microorganisms and neoplastic cells.
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Activated monocytes release a number of substances, including inflammatory cytokines and eicosanoids, that are highly toxic to cells of the central nervous system.
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Microglial activation is central to the inflammatory response in Alzheimer's Disease (AD).
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Microglia are immune system cells associated with Alzheimer's disease plaques containing beta-amyloid (A beta).
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Phospholipase A2 (PLA2) is the key enzyme that initiates the arachidonic acid cascade, which leads to the generation of multiple eicosanoid products.
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Interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), and interleukin-6 (IL-6) were measured in the cerebrospinal fluid (CSF) and plasma of 12 control subjects, 11 sporadic Alzheimer's disease (AD) and 22 de novo Parkinson's disease (PD) patients using high sensitivity enzyme-linked immunosorbent assays (ELISA).
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Alzheimer's disease is the most common cause of progressive intellectual failure.
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36/100
One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species.
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36/100
The origin of ramified microglia has been a longstanding controversial issue, with 4 major schools of thought, which state that they are derived (1) from invasion of mesodermal pial elements, (2) from neuroectodermal matrix cells together with the macroglia, (3) from pericytes, and (4) from invasion of monocytes in early development.
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Multiple sclerosis (MS) brain tissue, spleen, and PBMC were studied using immunocytochemistry and FACS for immunoreactivity for lymphotoxin (LT) and TNF.
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Frozen brain specimens from patients with multiple sclerosis (MS) and other neurologic diseases were analyzed using immunocytochemical techniques for the presence of TNF.
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Frozen brain specimens from eight multiple sclerosis (MS) patients were examined for the presence of leukocytes and their cell products by using a panel of monoclonal antibodies.
From across this tag
9 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 9. The same 9 appear here every time.
- A Therapeutic Strategy for Alzheimer's Disease Focused on Immune-inflammatory Modulation
- Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model
- A Multi-omic Atlas of Human Choroid Plexus in Alzheimer's Disease
- Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism
- TLR7-mediated autoimmunity targets Robo3 to drive astrogliosis in frontotemporal dementia
- Inflammasome activation and innate immunity in Alzheimer's disease
- The TREM2-DAP12 signaling pathway in Nasu-Hakola disease: a molecular genetics perspective
- Impaired microglial phagocytosis promotes seizure development
- Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE