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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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Strong evidence implicates the complement pathway as an important contributor to amyloid pathology in Alzheimer's disease (AD); however, the role of complement in tau modulation remains unclear.
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39/100
Alzheimer's disease (AD) is characterized by the progressive destruction and dysfunction of central neurons.
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There are currently no effective therapeutics for Alzheimer disease (AD).
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Gene ontology analyses coupled with bioinformatics approaches revealed drug targets and transcriptional regulators of microglial modules predicted to favorably modulate neuroinflammation in AD.
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These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases.
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Neurodegenerative diseases, the leading cause of morbidity and disability, are gaining increased attention as they impose a considerable socioeconomic impact, due in part to the ageing community.
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Innate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses.
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Microglia are emerging as key players in neurodegenerative diseases, such as Alzheimer's disease (AD).
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With a rapidly aging global human population, finding a cure for late onset neurodegenerative diseases has become an urgent enterprise.
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Individual reports suggest that the central nervous system (CNS) contains multiple immune cell types with diverse roles in tissue homeostasis, immune defense, and neurological diseases.
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Neuroinflammatory responses in Alzheimer's disease (AD) are complex and not fully understood.
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Alzheimer's disease (AD) is the most common form of dementia, an eversible, progressive disease that causes problems with memory, thinking, language, planning, and behavior.
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The spreading of pathology within and between brain areas is a hallmark of neurodegenerative disorders.
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Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS).
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There has been an explosion of new findings recently giving us insights into the involvement of microglia in central nervous system (CNS) disorders.
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41/100
To clarify the role of microglia in brain homeostasis and disease, an understanding of their maintenance, proliferation and turnover is essential.
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The complement cascade not only is an innate immune response that enables removal of pathogens but also plays an important role in microglia-mediated synaptic refinement during brain development.
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Here, we studied whether multiple sclerosis (MS) could be a complement to the CNS disorders that are associated with the GLP-1/GLP-1R signaling axis.
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Microglia play critical roles in brain development, homeostasis, and neurological disorders.
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Amyloid-β deposition, neuroinflammation and tau tangle formation all play a significant role in Alzheimer's disease.
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Activation of innate immunity and the assembly of microglial cells at sites of Alzheimer disease pathology has long been regarded as bystander phenomenon, which does not actively contribute to disease pathogenesis and progression.
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Mounting evidence suggests neuroinflammation is a key process in glaucoma, yet the precise roles are not known.
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The CNS is protected by the immune system, including cells that reside directly within the CNS and help to ensure proper neural function, as well as cells that traffic into the CNS with disease.
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70/100
These data suggest that resveratrol decreases CSF MMP9, modulates neuro-inflammation, and induces adaptive immunity.
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Alzheimer's disease (AD) is the most common form of dementia, which has been currently considered as a genetically complex disorder caused by a combination of environmental and genetic risk factors.
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Activation of the inflammasome is implicated in the pathogenesis of an increasing number of inflammatory diseases, including Alzheimer's disease (AD).
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Recent laboratory and gene sequencing data suggest that variations in receptors called the "triggering-receptors-expressed-on-myeloid-cells" (TREMs) are implicated in Alzheimer's disease, Parkinson's disease, multiple sclerosis, and frontotemporal lobar degeneration.
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39/100
Alzheimer disease (AD) is a progressive neurodegenerative disorder leading to cognitive decline, neuropsychiatric symptoms, disability, caregiver burden, and premature death.
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40/100
The concept of the inflammasome, a macromolecular complex sensing cell stress or danger signals and initiating inflammation, was first introduced approximately a decade ago.
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Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.
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Several attempts have been made to treat Alzheimer's disease (AD) using anti-amyloid strategies with disappointing results.
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The cytokine interleukin-6 (IL-6) plays a critical role in the pathogenesis of inflammatory disorders and in the physiological homeostasis of neural tissue.
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The blood-brain barrier (BBB) plays a key role in maintaining the specialized microenvironment of the central nervous system (CNS), and enabling communication with the systemic compartment.
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mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1β, IL-18) was up-regulated in severe and MILD AD.
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In addition to amyloid-β plaque and tau neurofibrillary tangle deposition, neuroinflammation is considered a key feature of Alzheimer's disease pathology.
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We show that inhibition of γ-secretase-dependent cleavage of the TREM2 C-terminal fragment in cellular membranes interferes with TREM2-dependent signaling and cellular function.
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Previously, we showed that overexpression of triggering receptor expressed on myeloid cells 2 (TREM2), a microglia-specific immune receptor, in the brain of a middle-aged (7 months old) APPswe/PS1dE9 mice could ameliorate Alzheimer's disease (AD)-related neuropathology by enhancement of microglial amyloid-β (Aβ) phagocytosis.
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Increasing evidence supports a role of neuroinflammation in the pathogenesis of Alzheimer's disease (AD).
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Inflammation may play a role in neural damage in preclinical AD.
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Recent genome-wide association studies implicate microglia in Alzheimer's disease (AD) pathogenesis; however, their biological significance remains poorly understood.
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Patients with chronic inflammation are often associated with the emergence of depression symptoms, while diagnosed depressed patients show increased levels of circulating cytokines.
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The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases.
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Despite decades of intensive research, the biological mechanisms that causally underlie depression are still unclear, and therefore the development of novel effective antidepressant treatments is hindered.
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Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease.
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41/100
Inflammation is a pathological hallmark of Alzheimer's disease, and innate immune cells have been shown to contribute to disease pathogenesis.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain, which is characterized by the formation of extracellular amyloid plaques (or senile plaques) and intracellular neurofibrillary tangles.
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Microglia serve key homeostatic roles, and respond to neuronal perturbation and decline with a high spatiotemporal resolution.
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Pathological aggregation of tau is a hallmark of Alzheimer’s disease and related tauopathies.
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Pathological conditions such as epilepsy cause misregulation of adult neural stem/progenitor populations in the adult hippocampus in mice, and the resulting abnormal neurogenesis leads to impairment in learning and memory.
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Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD).
From across this tag
10 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 10. The same 10 appear here every time.
- IRF3 regulates neuroinflammatory responses and the expression of genes associated with Alzheimer's disease
- Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
- Impaired microglial phagocytosis promotes seizure development
- PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology
- Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) R47H Variant Causes Distinct Age- and Sex-Dependent Musculoskeletal Alterations in Mice
- Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer
- Semaglutide attenuates neuroinflammation in male mice
- Role of neuroinflammation in neurodegeneration development
- Delivery of siRNA to the mouse brain by systemic injection of targeted exosomes
- Neuroinflammation as a Common Feature of Neurodegenerative Disorders