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Home › Research › Topics › nlrp3

nlrp3

384 studies tagged nlrp3, dated 1986-05-01 to 2026-11-01. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Molecular MRI of Neuroinflammation in Alzheimer's Disease using a Folate-targeted Nanoprobe 2026-11-01
  2. Neuroinflammation is an early pathological process in a mouse model of prodromal Parkinsons disease 2026-10-30
  3. The TREM-receptor family interactome in the human brain 2026-10-29

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.

  1. Molecular MRI of Neuroinflammation in Alzheimer's Disease using a Folate-targeted Nanoprobe

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-11-01 Inflammation and the immune system

    Microglial activation and FR expression in APP/PS1 and P301S transgenic mouse models of AD was measured using flow cytometry.

  2. Neuroinflammation is an early pathological process in a mouse model of prodromal Parkinsons disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Mild cognitive impairment

    Approximately 90% of Parkinson's disease (PD) patients exhibit olfactory deficits, which often precedes motor symptoms by years, and are a robust predictor for PD and subsequent cognitive decline.

  3. The TREM-receptor family interactome in the human brain

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-29 Genetics

    The Triggering Receptors Expressed on Myeloid cells (TREMs) are a family of cell-surface receptors instrumental in the activation of different myeloid cells.

  4. A Binding Site for CVN293 Reveals a Mechanism for Allosteric Control of THIK-1 K2P Channel Gating

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-28 Inflammation and the immune system

    Microglial activation and subsequent neuroinflammation involves THIK-1 (KCNK13), a Two-Pore Domain (K2P) K+ channel.

  5. Soluble TREM2 suppresses neuronal activity

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-28 TREM2 and immune genetics

    Neuronal activity must be tightly controlled to maintain brain function.

  6. High-content imaging of live microglia-containing Alzheimer’s disease brain organoids

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27 Inflammation and the immune system

    This method establishes a platform for high-throughput longitudinal drug screening in immunocompetent human COs that will enable the identification of new therapeutic candidates to modulate Aβ aggregation, glial reactivity, and neurodegeneration.

  7. Ms4a4a loss preferentially remodels microglia with limited, compartment-specific effects across central and peripheral immune compartments in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27 Genetics

    These findings identify microglia as the immune population most strongly remodeled by Ms4a4a loss in the setting of amyloid pathology.

  8. Discovery of a brain-penetrant CHI3L1 inhibitor as an oral modulator of neuroinflammation in Alzheimers disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-21 Tau biomarkers

    Chitinase-3-like protein 1 (CHI3L1) is elevated in Alzheimers disease (AD), but its role in glial dysfunction and therapeutic tractability remain unclear.

  9. Astrocytic sEH–EET signaling regulates microglial lysosomal function and suppresses the STING–Type I interferon pathway in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20 Inflammation and the immune system

    We define an astrocyte–microglia axis in which astrocytic sEH limits EET availability and thereby sustains microglial STING signaling.

  10. Protective or Pathogenic? Microglial Responses at the Intersection of Amyloid-β, Tau, and Neuroinflammation in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-20 Inflammation and the immune system

    Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, pathological tau aggregation, and neuronal loss.

  11. Electroacupuncture alleviate cognitive impairment via activation of TREM2-positive microglia in APP/PS1 mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-16 TREM2 and immune genetics

    EA ameliorated cognitive impairment in APP/PS1 mice by enhancing TREM2⁺ microglia-mediated Aβ clearance and suppressing neuroinflammation. scRNA-seq further revealed that EA reshaped microglial transcriptional states and intercellular communication networks in a TREM2-dependent manner.

  12. Progranulin deficiency promotes neuroinflammation through cathepsin B-mediated activation of the NLRP3 inflammasome

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13 Drug development

    Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation.

  13. A rapid, genetically-tractable human iPSC-derived model for studying tissue-resident macrophage biology in Alzheimer’s and other diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12 Genetics

    Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer’s disease (AD).

  14. Mechanistic study of PHLDA1 in cognitive dysfunction of Alzheimer’s disease model mice via FoxO1‑mediated neuroinflammation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12 Biomarkers

    Neuroinflammation is a core driver of Alzheimer’s disease (AD) progression.

  15. DAP12-deficient microglia adopt a TREM2-independent antigen-presenting state with a glial-to-neuronal cascade in Nasu-Hakola disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-11 TREM2 and immune genetics

    Nasu-Hakola disease (NHD), a dementia with about 200 cases worldwide, is caused by loss-of-function mutation of TYROBP , encoding DAP12, or its receptor TREM2 .

  16. ASC specks and α-synuclein amplify microglial NLRP3 inflammasome activation and co-localize with Lewy body pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-10 Brain tissue and pathology

    Neuroinflammation is a hallmark of several chronic neurodegenerative disorders, including Parkinson’s disease (PD) and other synucleinopathies, and is closely associated with microglial activation.

  17. Human multiscale transcriptomics identifies the NLRP3 inflammasome as a convergent druggable target in Alzheimer’s disease: validation with dimethyl itaconate in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-07 Brain tissue and pathology

    Neuroinflammation is a hallmark of Alzheimer’s disease (AD); however, which neuroinflammatory effectors are consistently altered across independent human cohorts, brain regions, and microglial states—and can be engaged by available compounds—remains incompletely defined.

  18. TLR7-mediated autoimmunity targets Robo3 to drive astrogliosis in frontotemporal dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-07 Disease mechanisms

    Mutations in GRN and C9orf72 are common causes of frontotemporal dementia (FTD).

  19. Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Clinical and translational medicine 2026-10 TREM2 and immune genetics

    We address translation bottlenecks-including blood-brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation-outlining a biomarker-guided, context-tailored precision therapeutic framework for targeting the TREM2 axis.

  20. Plasma immune signatures associate with neurodegeneration in frontotemporal lobar degeneration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-29 Biomarkers

    In exploratory full-cohort models, the multivariate CNS signature achieved an area under the curve of 0.93, compared with 0.82 for the multivariate inflammation signature.

  21. Extracellular CIRP induces neurotoxic astrocytes via TREM-1 in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24 Biomarkers

    Extracellular cold-inducible RNA-binding protein (eCIRP) is a crucial neuroinflammatory mediator in ischemic stroke and alcohol-induced memory impairment.

  22. A self-limiting, TREM2-dependent anabolic program confers microglial resilience in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20 TREM2 and immune genetics

    Microglia are key drivers of Alzheimer’s disease (AD), and TREM2, one of the strongest genetic risk factors, enables the disease-associated microglia (DAM) state required for plaque engagement.

  23. A sphingomyelin-cholesterol complex regulates TLR4 activation in microglia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14 TREM2 and immune genetics

    Microglial activation in response to lipopolysaccharide (LPS) requires Toll-like receptor 4 (TLR4) redistribution into cholesterol- and sphingolipid-rich membrane domains, yet the lipid determinants of this process remain unclear.

  24. Brain-resident myeloid cells promote rapid leukocyte adhesion in leptomeningeal vessels after anti-Aβ immunotherapy

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-11 Treatments

    Anti-amyloid-β (Aβ) immunotherapy improves cognitive outcomes in Alzheimer’s disease (AD) but is associated with amyloid-related imaging abnormalities (ARIA), through poorly understood mechanisms.

  25. The TREM2 targeting small molecule Sob-AM2 improves cognition independent of Aβ plaque alteration in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-05 TREM2 and immune genetics

    These results suggest that the cognitive-enhancing effects of Sob-AM2 are not the result of reduced overall plaque burden.

  26. APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-31 TREM2 and immune genetics

    Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology.

  27. MicroRNA-223 Enhances Microglia-Dependent Clearance of Amyloid Beta Plaques and Ameliorates Behavioral Deficits in a Mouse Model of Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-23 TREM2 and immune genetics

    The Alzheimer’s disease (AD) brain is characterized by dysregulated expression of multiple microRNAs (miRNA), positioning them as promising diagnostic and therapeutic targets.

  28. Photobiomodulation of immune crosstalk rescues neuroinflammation in Alzheimer's disease models

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain : a journal of neurology 2026-07-23 Inflammation and the immune system

    Peripheral immune cell infiltration and crosstalk with brain-resident cells critically drive Alzheimer's disease (AD)-associated neuroinflammation, highlighting its therapeutic potential.

  29. Immunoproteasome Deficiency Impairs Microglial Clearance and Worsens Tau and Amyloid Pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-20 TREM2 and immune genetics

    Immunoproteasome induction is prominent in Alzheimer’s disease (AD), but whether it protects proteostasis or amplifies neuroinflammation remains unresolved.

  30. A non-canonical androgen signaling pathway drives microglial activation and tau pathology in females

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-16 TREM2 and immune genetics

    Alzheimer's disease (AD) disproportionately affects women, who exhibit greater vulnerability to Tau pathology and neuroinflammation.

  31. The Microglial Protein sTREM2 Inhibits the Bacterial Functional Amyloid CsgA and Suppresses Amyloid-Dependent Biofilm Formation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-06 TREM2 and immune genetics

    Protein misfolding and aggregation, including amyloid fibril formation, underlie a large class of human diseases including prominent neurological disorders such as Alzheimer’s and Parkinson’s disease.

  32. Neuroinflammation and Tauopathies

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular biology reports 2026-06-30 Inflammation and the immune system

    Alzheimer's disease (AD) and related Tauopathies are neurodegenerative disorders characterized by the accumulation of hyperphosphorylated Tau protein in neurofibrillary tangles and frequently accompanied by amyloid-β (Aβ) pathology.1 While Tau aggregation has long been considered a primary driver of neurodegeneration, growing evidence highlights neuroinflammation as a central and early contributor to disease onset and progression.

  33. Semaglutide attenuates neuroinflammation in male mice

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature communications 2026-06-09 Drug development

    Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation.

  34. Peripheral biomarkers of neuroinflammation in Alzheimer's disease and vascular dementia

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Biochemical pharmacology 2026-05-17 Inflammation and the immune system

    Alzheimer's disease (AD) and vascular dementia (VaD) are the two commonest causes of dementia in older adults and frequently coexist as mixed neurodegenerative-cerebrovascular pathology.

  35. HDAC6 regulates BACE1 stability and NLRP3 inflammasome activation in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain : a journal of neurology 2026-03-06 Inflammation and the immune system

    Alzheimer's disease (AD) is marked by amyloid-β (Aβ) accumulation, tau pathology, and neuroinflammation.

  36. TREM2 in neurodegeneration and diseases

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular psychiatry 2026-03-06 TREM2 and immune genetics

    Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS).

  37. Phagocytes as plaque catalysts: Human macrophages generate seeding-competent Aβ42 fibrils with cross-seeding activity

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2026-03-02 TREM2 and immune genetics

    The prevailing view frames microglia and macrophages as guardians against amyloid beta (Aβ) accumulation in Alzheimer's disease (AD).

  38. Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of clinical investigation 2026-02-24 Inflammation and the immune system

    Mild traumatic brain injury (mTBI) from a closed-head injury (CHI) can lead to prevalent neuropsychiatric disorders, including mood disorders and an increased risk for neurodegenerative diseases and dementia.

  39. Microglia TFEB activation attenuates Alzheimer's disease pathology by enhancing autophagy-lysosomal function

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of neuroinflammation 2026-02-11 Inflammation and the immune system

    Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation, neuroinflammation, synaptic dysfunction, and cognitive decline.

  40. TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonism

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature communications 2026-01-24 TREM2 and immune genetics

    Triggering receptor expressed on myeloid cells 2 (TREM2) is a central regulator of microglial activity and loss-of-function coding variants are major risk factors for late onset Alzheimer's disease (LOAD).

  41. Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature communications 2026-01-22 Inflammation and the immune system

    Chlamydia pneumoniae is an intracellular bacterium implicated in Alzheimer's disease (AD), but its role in retinal pathology and disease progression is unclear.

  42. Semaglutide Attenuates Neuroinflammation in Mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-01-12 Drug development

    Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation.

  43. The Alzheimer's disease risk genes MS4A4A and MS4A6A cooperate to negatively regulate TREM2 and microglia states

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neuron 2025-12-22 TREM2 and immune genetics

    Genetic variations in MS4A4A and MS4A6A Triggering receptor expressed on myeloid cells 2 (TREM2) are linked to the regulation of cerebrospinal-fluid-soluble TREM2 levels and are associated with Alzheimer's disease (AD) risk and progression.

  44. Trem2R47H and reduced TREM2 expression both mimic human Alzheimer's disease signatures in mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-12-19 TREM2 and immune genetics

    Trem2*R47H mice had alternative splicing leading to reduced Trem2 expression; Trem2*R47HHSS mice expressed Trem2 at wild-type transcript and protein levels.

  45. A Multi-omic Atlas of Human Choroid Plexus in Alzheimer's Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-12-17 Genetics

    The choroid plexus (CP) regulates barrier integrity, cerebrospinal-fluid (CSF) dynamics, and immune surveillance, yet its role in Alzheimer's disease (AD) remains poorly defined.

  46. Microglial clearance, neuroprotection and cognitive recovery via a novel synthetic sulfolipid in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuroinflammation 2025-12-13 TREM2 and immune genetics

    We demonstrate that the small-molecule TREM2 ligand SULF A functions as an immunomodulator that reprograms microglia toward a reparative phenotype.

  47. As48, a first-in-class dual-function TREM2 modulator: Receptor activation and shedding inhibition

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2025-12-02 TREM2 and immune genetics

    Triggering receptor expressed on myeloid cells 2 (TREM2) dysfunction contributes to Alzheimer's disease pathogenesis, yet current therapeutics cannot prevent ADAM-mediated receptor shedding that diminishes signaling efficacy.

  48. Enhancing Tyro3 signaling ameliorates IL-1β production through STAT1 in Alzheimer's disease models

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of leukocyte biology 2025-12-01 Inflammation and the immune system

    Neuroinflammation plays a vital role in determining the trajectory of Alzheimer's disease (AD) progression.

  49. TREM2 Alleviates Neuroinflammation and Improves Neurogenesis in ApoE-/- Mice by Regulating M1/M2 Microglial Polarization

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular neurobiology 2025-11-20 TREM2 and immune genetics

    Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor abundantly expressed in microglia in the brain.

  50. Role of TREM2 in neuroinflammation

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Experimental neurology 2025-11-08 TREM2 and immune genetics

    Triggering receptor expressed on myeloid cells 2 (TREM2) is cell surface transmembrane receptor of the TREM family, predominantly expressed on microglia within the central nervous system (CNS).

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.

All topic tags with their study counts