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inflammasome
384 studies tagged inflammasome, 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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This is the first demonstration of TLR4-dependent upregulation of cytokines in an AD mouse model.
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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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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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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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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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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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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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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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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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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
8 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 8. The same 8 appear here every time.
- Enhancing TREM2 expression activates microglia and modestly mitigates tau pathology and neurodegeneration
- Effect of stress and peripheral immune activation on astrocyte activation in transgenic bioluminescent Gfap‐luc mice
- Protective or Pathogenic? Microglial Responses at the Intersection of Amyloid-β, Tau, and Neuroinflammation in Alzheimer’s Disease
- SIRT1 Deficiency in Microglia Contributes to Cognitive Decline in Aging and Neurodegeneration via Epigenetic Regulation of IL-1β
- ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease
- Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer's disease
- Restoring metabolism of myeloid cells reverses cognitive decline in ageing
- Extracellular CIRP induces neurotoxic astrocytes via TREM-1 in Alzheimer’s disease