ArticleNeurobiology of disease2014
Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- ZFP36-mediated ZBP1 degradation inhibits microglia pro-inflammatory and NLRP3 inflammasome activation in Alzheimer's disease.Cell biology and toxicology · 2026Article
- How Many Alzheimer-Perusini's Atypical Forms Do We Still Have to Discover?Biomedicines · 2023Review
- Neuroprotective Effect of Quercetin and Memantine against AlClMolecules (Basel, Switzerland) · 2023Article
- Microglia in Alzheimer's Disease: a Key Player in the Transition Between Homeostasis and Pathogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Functional and Phenotypic Diversity of Microglia: Implication for Microglia-Based Therapies for Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Targeting innate immunity to protect and cure Alzheimer's disease: opportunities and pitfalls.Molecular psychiatry · 2021Review
- An overview of microglia ontogeny and maturation in the homeostatic and pathological brain.The European journal of neuroscience · 2021Review
- Effects of concentrated ambient ultrafine particulate matter on hallmarks of Alzheimer's disease in the 3xTgAD mouse model.Neurotoxicology · 2021Article
- Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition.Journal of neuroinflammation · 2020Article
- Evaluating the Effect of Interleukin-4 in the 3xTg Mouse Model of Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia.Journal of neuroinflammation · 2019Article
- Amelioration of Alzheimer's disease pathology and cognitive deficits by immunomodulatory agents in animal models of Alzheimer's disease.Neural regeneration research · 2019Article
- Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease.Journal of neuroinflammation · 2019Review
- Article
- Inflammasomes as therapeutic targets for Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2017Review
- Candidate SNP Markers of Familial and Sporadic Alzheimer's Diseases Are Predicted by a Significant Change in the Affinity of TATA-Binding Protein for Human Gene Promoters.Frontiers in aging neuroscience · 2017Article
- Targeting innate immunity for neurodegenerative disorders of the central nervous system.Journal of neurochemistry · 2016Review
- Neuroprotective effects of tetrandrine against vascular dementia.Neural regeneration research · 2016Article
- CX3CL1/CX3CR1 in Alzheimer's Disease: A Target for Neuroprotection.BioMed research international · 2016Review
- Arginase 1+ microglia reduce Aβ plaque deposition during IL-1β-dependent neuroinflammation.Journal of neuroinflammation · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is a key component of Alzheimer's disease (AD) pathogenesis. Particularly, the proinflammatory cytokine interleukin-1 beta (IL-1β) is upregulated in human AD and believed to promote amyloid plaque deposition. However, studies from our laboratory have shown that chronic IL-1β overexpression in the APPswe/PSEN1dE9 (APP/PS1) mouse model of AD ameliorates amyloid pathology, increases plaque-associated microglia, and induces recruitment of peripheral immune cells to the brain parenchyma. To investigate the contribution of CCR2 signaling in IL-1β-mediated amyloid plaque clearance, seven month-old APP/PS1/CCR2(-/-) mice were intrahippocampally transduced with a recombinant adeno-associated virus serotype 2 containing the cleaved form of human IL-1β (rAAV2-IL-1β). Four weeks after rAAV2-IL-1β transduction, we found significant reductions in 6E10 and Congo red staining of amyloid plaques that was confirmed by decreased levels of insoluble Aβ1-42 and Aβ1-40 in the inflamed hippocampus. Bone marrow chimeric studies confirmed the presence of infiltrating immune cells following IL-1β overexpression and revealed that dramatic reduction of CCR2(+) peripheral mononuclear cell recruitment to the inflamed hippocampus did not prevent the ability of IL-1β to induce amyloid plaque clearance. These results suggest that infiltrating CCR2(+) monocytes do not contribute to IL-1β-mediated amyloid plaque clearance.
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Registered trials
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.