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nlrp3
384 studies tagged nlrp3, 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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The aim of this review is to explore the role of NLRP3 activation-mediated neuronal pyroptosis and neuroinflammation in neurodegenerative diseases.
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Alzheimer's disease (AD) is the most prevalent cause of dementia worldwide.
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Neuroinflammation is a key pathological feature in neurological diseases, including Alzheimer's disease (AD).
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Altered microglial states affect neuroinflammation, neurodegeneration, and disease but remain poorly understood.
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Amyloid plaques are considered to be the pathological hallmark of Alzheimer's disease (AD).
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Colony-stimulating factor-1 receptor (CSF-1R)-related leukoencephalopathy (CRL) is a neurodegenerative disease that triggers early demyelination, leading to an adult-onset dementia.
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Studies in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Amyotrophic lateral sclerosis, Huntington's disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process.
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41/100
Alzheimer's disease (AD), also known as senile dementia, is the most common degenerative disease of the central nervous system.
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Microglia, the macrophages of the brain, are vital for brain homeostasis and have been implicated in a broad range of brain disorders.
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Recent studies showed increased expression of complements in various neurodegenerative diseases, including Alzheimer's and Parkinson's diseases.
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Mutations in a microglia-associated gene TREM2 increase the risk of Alzheimer's disease.
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Alzheimer's Disease is the most common form of dementia; its key pathological findings include the deposition of extracellular-neurotoxic-plaques composed of amyloid-beta (Ab).
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CUMS induced depressive-like behaviors and cognitive decline in mice, which could be reversed by inhibiting NLRP3 inflammasome.
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Previously, we reported that H157Y, a rare coding variant on exon 3 of the triggering receptor expressed on myeloid cells 2 gene (TREM2), was associated with Alzheimer's disease (AD) risk in a Han Chinese population.
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During the 4-day meeting, presenters illuminated aspects of the cross-talk between APOE and immunity, with a focus on the roles of microglia, triggering receptor expressed on myeloid cells 2 (TREM2), and components of inflammation (e.g., tumor necrosis factor α [TNFα]).
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Alzheimer's disease (AD) is associated with the cerebral deposition of Amyloid-β (Aβ) peptide, which leads to NLRP3 inflammasome activation and subsequent release of interleukin-1β (IL-1β) and interleukin-18 (IL-18).
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In activated microglia, cholesterol enrichment promoted the release of encapsulated IL-1β accompanied by a switch to a more neuroprotective phenotype, with increased phagocytic capacity and release of neurotrophic factors.
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β2-Microglobulin (β2M), a component of the major histocompatibility complex class I molecule, is associated with aging-related cognitive impairment and Alzheimer's disease.
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Microglia and neuroinflammation are implicated in the development and progression of Alzheimer's disease (AD).
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Translocase of outer mitochondrial membrane 40 (TOMM40) is located in the outer membrane of mitochondria.
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Expansion of the hexanucleotide repeat GGGGCC in the C9orf72 gene is the most common genetic factor in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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The complement system is an ancient collection of proteolytic cascades with well-described roles in regulation of innate and adaptive immunity.
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Alzheimer's disease (AD) is characterized by synaptic loss, which can result from dysfunctional microglial phagocytosis and complement activation.
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Consistent with previous in vitro findings, Trem2 H157Y increases TREM2 shedding with elevated soluble TREM2 levels in the brain and serum.
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Current hypothesis of Alzheimer's disease (AD) postulates that amyloid β (Aβ) deposition in the brain causes tau inclusion in neurons and leads to cognitive decline.
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The major neuropathological hallmarks of Alzheimer's disease (AD) are amyloid β (Aβ) plaques and neurofibrillary tangles (NFT), accompanied by neuroinflammation and neuronal loss.
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Adult neurogenesis occurs mainly in the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles.
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Brain iron accumulation, which is indicated in the cerebrospinal fluid (CSF) ferritin, is associated with the development of Alzheimer's Disease (AD).
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Synapses are bridges for information transmission in the central nervous system (CNS), and synaptic plasticity is fundamental for the normal function of synapses, contributing substantially to learning and memory.
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Traumatic brain injury (TBI) promotes several Alzheimer's disease-like pathological features, including microtubule-associated protein tau (MAPT) accumulation within neurons.
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There is a huge need for novel therapeutic and preventative approaches to Alzheimer's disease (AD) and neuroinflammation seems to be one of the most fascinating solutions.
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Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer's disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy economic burden on families and society.
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Traditionally, lymphocytic interferon γ (IFN-γ) was considered to be a simple 'booster' of proinflammatory responses by microglia (brain-resident macrophages) during bacterial or viral infection.
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TREM2 (Triggering receptor expressed on myeloid cells 2) is the causative gene for Nasu-Hakola disease, which is characterized by multiple bone cysts and leukoencephalopathy.
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Alzheimer's disease is one of the most common age-related neurodegenerative disorders.
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Cancer continues to be a substantial health concern and a leading cause of death in the United States and around the world.
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Alzheimer's disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge.
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Pg OMVs impaired memory and learning ability of mice and decreased tight junction-related gene expression ZO-1, occludin, claudin-5, and occludin protein expression in the hippocampus.
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The receptor Triggering Receptor Expressed on Myeloid cells 2 (TREM2) is associated with several neurodegenerative diseases including Alzheimer's Disease and TREM2 stimulation represents a novel therapeutic opportunity.
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Oral treatment of the amyloid prone AD-like APPPS1 mice with spermidine reduced neurotoxic soluble Aβ and decreased AD-associated neuroinflammation.
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Microglia are critical in brain development and Alzheimer's disease (AD) etiology.
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Neuroinflammation is a hallmark of many neurodegenerative diseases (NDs) and plays a fundamental role in mediating the onset and progression of disease.
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Parkinson's disease (PD) is a progressive neurological disorder marked by cardinal clinical symptoms such as rigor, tremor, and akinesia.
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These results indicate that the compromised function of microglia in AD could be improved by controlled activation of PIEZO1 channels resulting in alleviated Aβ burden.
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Alzheimer's disease (AD) is a neurodegenerative disorder molecularly characterized by the formation of amyloid β (Aβ) plaques and type 2 microtubule-associated protein (Tau) abnormalities.
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Previous studies proposed the Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a receptor expressed in myeloid cells including microglia in brain and osteoclasts in bone, as a link between brain and bone disease.
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Neuroinflammation is considered one of major factors in the pathogenesis of Alzheimer's disease (AD).
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Microglia are the resident macrophages of the central nervous system.
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Dementia with Lewy bodies (DLB) is the second most common neurodegenerative cause of dementia, behind Alzheimer's disease (AD).
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The pro-inflammatory activation of microglia is a hallmark of Alzheimer's disease (AD), and this process involves a switch from oxidative phosphorylation (OXPHOS) toward glycolysis.
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.
- Progranulin deficiency promotes neuroinflammation through cathepsin B-mediated activation of the NLRP3 inflammasome
- Neuroinflammation and Tauopathies
- TREM2 in neurodegeneration and diseases
- ASC specks and α-synuclein amplify microglial NLRP3 inflammasome activation and co-localize with Lewy body pathology
- Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain
- Key Mechanisms and Potential Targets of the NLRP3 Inflammasome in Neurodegenerative Diseases
- Interleukin 1 in the brain: biology, pathology and therapeutic target
- A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases