ArticleThe American journal of pathology2001
Abeta-induced inflammatory processes in microglia cells of APP23 transgenic mice.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 202 citations in OpenAlex.
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- Dual orexin receptor antagonism with lemborexant enhances microglial clearance of β-amyloid in mice.Molecular neurodegeneration · 2026Article
- "Micro-managing" immune activation and protein turnover: microglial lysosomes in the context of health and disease.NPJ dementia · 2026Review
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- Single-nucleus transcriptomics reveals a distinct microglial state and increased MSR1-mediated phagocytosis as common features across dementia subtypes.Genome medicine · 2025Article
- Sex-specific changes in energy demand during the preplaque stage in a transgenic Alzheimer's mouse model.Biology of sex differences · 2025Article
- Exploring temporal and sex-linked dysregulation in Alzheimer disease phosphoproteome.iScience · 2024Article
- Inflammasome assembly in neurodegenerative diseases.Trends in neurosciences · 2023Review
- Effects of Probiotics on Colitis-Induced Exacerbation of Alzheimer's Disease inInternational journal of molecular sciences · 2023Article
- Cerebral Superficial Siderosis : Etiology, Neuroradiological Features and Clinical Findings.Clinical neuroradiology · 2023Review
- Mitochondrial dynamics in macrophages: divide to conquer or unite to survive?Biochemical Society transactions · 2023Article
- BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia.Molecular neurodegeneration · 2022Article
- Microglia in Alzheimer's Disease: A Favorable Cellular Target to Ameliorate Alzheimer's Pathogenesis.Mediators of inflammation · 2022Review
- Mental Illness and Amyloid: A Scoping Review of Scientific Evidence over the Last 10 Years (2011 to 2021).Brain sciences · 2021Article
- The role of macrophage scavenger receptor 1 (Msr1) in prion pathogenesis.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Alzheimer's Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia.International journal of molecular sciences · 2021Review
- Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2021Article
- Distinct microglial response against Alzheimer's amyloid and tau pathologies characterized by P2Y12 receptor.Brain communications · 2021Article
- Association of naturally occurring antibodies to β-amyloid with cognitive decline and cerebral amyloidosis in Alzheimer's disease.Science advances · 2021Article
- Interleukin-12/23 deficiency differentially affects pathology in male and female Alzheimer's disease-like mice.EMBO reports · 2020Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A microglial response is part of the inflammatory processes in Alzheimer's disease (AD). We have used APP23 transgenic mice overexpressing human amyloid precursor protein with the Swedish mutation to characterize this microglia response to amyloid deposits in aged mice. Analyses with MAC-1 and F4/80 antibodies as well as in vivo labeling with bromodeoxyuridine demonstrate that microglia in the plaque vicinity are in an activated state and that proliferation contributes to their accumulation at the plaque periphery. The amyloid-induced microglia activation may be mediated by scavenger receptor A, which is generally elevated, whereas the increased immunostaining of the receptor for advanced glycation end products is more restricted. Although components of the phagocytic machinery such as macrosialin and Fc receptors are increased in activated microglia, efficient clearance of amyloid is missing seemingly because of the lack of amyloid-bound autoantibodies. Similarly, although up-regulation of major histocompatibility complex class II (IA) points toward an intact antigen-presenting function of microglia, lack of T and B lymphocytes does not indicate a cell-mediated immune response in the brains of APP23 mice. The similar characteristics of microglia in the APP23 mice and in AD render the mouse model suitable to study the role of inflammatory processes during AD pathogenesis.
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