ArticleCell death & disease2020
NLRP3-dependent microglial training impaired the clearance of amyloid-beta and aggravated the cognitive decline in Alzheimer's disease.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Mechanisms of Brain Aging and Their Links to Alzheimer's and Parkinson's Disease Pathology.International journal of molecular sciences · 2026Review
- Discovery of a brain penetrant NLRP3 inflammasome inhibitor that reduces neuropathic pain in mice.European journal of medicinal chemistry · 2026Article
- Distinct and combined interferon-ɑ/β-receptor-1 loss in neurons and astrocytes disrupt brain energy metabolism and drive Parkinsonian dementia.Journal of biomedical science · 2026Article
- Impact of Semaglutide on Hippocampal Injury in a Streptozotocin-Induced Model of Alzheimer's Disease.Biomedicines · 2026Article
- Targeting the HDAC4-NHE6-endosomal pH axis restores amyloid-β clearance and cognitive function in Alzheimer's disease mice.Journal of nanobiotechnology · 2026Article
- PANoptosis in neurological disorders: from inflammatory cell death mechanisms to neuroprotective strategies.Frontiers in neuroscience · 2026Review
- Therapeutic Potential of MCC950 in Restoring Autophagy and Cognitive Function in STZ-Induced Rat Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Suppression of NF-κB/NLRP3 by nanoligomer therapy mitigates ethanol and advanced age-related neuroinflammation.Journal of leukocyte biology · 2025Article
- Role of NLRP3 Inflammasome in Chronic Pain and Alzheimer's Disease-A Review.Journal of biochemical and molecular toxicology · 2025Review
- Biological and therapeutic significance of targeting NLRP3 inflammasome in the brain and the current efforts to develop brain-penetrant inhibitors.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Traditional Chinese medicine's holistic approach: regulating microglia-driven neuroinflammation for the resolution of Alzheimer's disease.Frontiers in cellular neuroscience · 2025Review
- MSC-Derived Extracellular Vesicles Alleviate NLRP3/GSDMD-Mediated Neuroinflammation in Mouse Model of Sporadic Alzheimer's Disease.Molecular neurobiology · 2024Article
- Diagnostic implications of ubiquitination-related gene signatures in Alzheimer's disease.Scientific reports · 2024Article
- NF-κB/NLRP3 Translational Inhibition by Nanoligomer Therapy Mitigates Ethanol and Advanced Age-Related Neuroinflammation.bioRxiv : the preprint server for biology · 2024Article
- Cortical microinfarcts potentiate recurrent ischemic injury through NLRP3-dependent trained immunity.Cell death & disease · 2024Article
- Design and Discovery of Novel NLRP3 Inhibitors and PET Imaging Radiotracers Based on a 1,2,3-Triazole-Bearing Scaffold.Journal of medicinal chemistry · 2024Article
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- Targeting NLRP3 inflammasome for neurodegenerative disorders.Molecular psychiatry · 2023Review
- Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023Review
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common form of dementia, is marked by progressive cognitive decline, deposition of misfolded amyloid-β (Aβ) peptide and formation of neurofibrillary tangles. Recently, microglial training has emerged as an important contributor to neurological diseases, which augments the subsequent inflammation. However, how it affects the pathology of AD remains unknown. Here, using a mouse model of sporadic Alzheimer's disease (SAD) induced by streptozotocin injection, we demonstrated that microglial training exacerbated Aβ accumulation, neuronal loss, and cognitive impairment. In addition, we injected MCC950 to inhibit NLRP3 activation and used an inducible Cre recombinase to delete the NLRP3 gene in microglia. Inhibition or depletion of microglial NLRP3 could protect against the pathologies of SAD and abolish the effects of microglial training. Our results identified microglial training as an important modifier of neuropathology in SAD and demonstrated that activation of NLRP3 inflammasome contributed to the pathologies and microglial training in SAD. Therefore, NLRP3 could be a potential therapeutic target for SAD treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.