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Microglial Receptor for Advanced Glycation End Product-Dependent Signal Pathway Drives β-Amyloid-Induced Synaptic Depression and Long-Term Depression Impairment in Entorhinal Cortex
Open accessAbstract
Overproduction of β-amyloid (Aβ) is a pathologic feature of Alzheimer's disease, leading to cognitive impairment. Here, we investigated the impact of cell-specific receptor for advanced glycation end products (RAGE) on Aβ-induced entorhinal cortex (EC) synaptic dysfunction. We found both a transient depression of basal synaptic transmission and inhibition of long-term depression (LTD) after the application of Aβ in EC slices. Synaptic depression and LTD impairment induced by Aβ were rescued by functional suppression of RAGE. Remarkably, the rescue was only observed in slices from mice expressing a defective form of RAGE targeted to microglia, but not in slices from mice expressing defective RAGE targeted to neurons. Moreover, we found that the inflammatory cytokine IL-1β (interleukin-1β) and stress-activated kinases [p38 MAPK (p38 mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase)] were significantly altered and involved in RAGE signaling pathways depending on RAGE expression in neuron or microglia. These findings suggest a prominent role of microglial RAGE signaling in Aβ-induced EC synaptic dysfunction.
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“AGEs and the receptor for advanced glycation end-products (RAGE) can play an important role in AD pathogenesis as higher levels of RAGE expression in neuronal, microglial, and endothelial cells in patients with AD compared with age-matched, non- demented controls are found [43,44,45,46].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [44]
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“Binding of Aβ to the microglial SR-J1 (also called RAGE) activates MAPK and NF-κB and contributes to synaptic dysfunction through IL-1β release in 2- to 3-month-old animals139.”
From Microglia in neurodegeneration (2018) · cites this paper as [139]
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“Furthermore, AGEs cross-linked with Aβ can also decrease the ability of microglia to clear plaques113.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [113]
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Metadata
- Authors
- Origlia, N., Bonadonna, C., Rosellini, A., Leznik, E., Arancio, O., Yan, S. S., & Domenici, L.
- Affiliations
- Neuroscience Institute (IT)
- Columbia University (US)
- University of L'Aquila (IT)
- Corresponding author
- Domenici, Luciano
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-08-25
- Volume
- 30
- Issue
- 34
- Pages
- 11414-11425
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3842472
- OpenAlex
- W2015426193
- Cited by
- 111
- References
- 82
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 9 · 2022: 11 · 2021: 10 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 10 · 2016: 5 · 2015: 6 · 2014: 13 · 2013: 7 · 2012: 8
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- KU ScholarWorks (University of Kansas) (submittedVersion, other-oa)
- Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion)
- Funders
- American Health Assistance Foundation
- Regione Toscana
- National Institutes of Health
- National Institute on Aging (P01AG017490, P01 AG 17490)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- receptor for advanced glycation end products, RAGE, amyloid-beta, Alzheimer's disease, entorhinal cortex, synaptic depression, long-term depression, microglia, synaptic dysfunction, IL-1β, p38 MAPK, JNK, neuroinflammation
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Mice, Inbred C57BL, Mice, Transgenic, Neural Inhibition, Receptors, Immunologic, Signal Transduction, Amyloid beta-Peptides, Glycation End Products, Advanced, Microglia, Mice, Knockout, Entorhinal Cortex, Long-Term Synaptic Depression, Mice
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