Receptor for advanced glycation end products mediates sepsis-triggered amyloid-β accumulation, Tau phosphorylation, and cognitive impairment
Open accessAbstract
Patients recovering from sepsis have higher rates of CNS morbidities associated with long-lasting impairment of cognitive functions, including neurodegenerative diseases.However, the molecular etiology of these sepsis-induced impairments is unclear.Here, we investigated the role of the receptor for advanced glycation end products (RAGE) in neuroinflammation, neurodegeneration-associated changes, and cognitive dysfunction arising after sepsis recovery.Adult Wistar rats underwent cecal ligation and perforation (CLP), and serum and brain (hippocampus and prefrontal cortex) samples were obtained at days 1, 15, and 30 after the CLP.We examined these samples for systemic and brain inflammation; amyloid- peptide (A) and Ser-202-phosphorylated Tau (p-Tau Ser-202 ) levels; and RAGE, RAGE ligands, and RAGE intracellular signaling.Serum markers associated with the acute proinflammatory phase of sepsis (TNF␣, IL-1, and IL-6) rapidly increased and then progressively decreased during the 30-day period post-CLP, concomitant with a progressive increase in RAGE ligands (S100B, N⑀-[carboxymethyl]lysine, HSP70, and HMGB1).In the brain, levels of RAGE and Toll-like receptor 4, glial fibrillary acidic protein and neuronal nitric-oxide synthase, and A and p-Tau Ser-202 also increased during that time.Of note, intracerebral injection of RAGE antibody into the hippocampus at days 15, 17, and 19 post-CLP reduced A and p-Tau Ser-202 accumulation, Akt/mechanistic target of rapamycin signaling, levels of ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein, and behavioral deficits associated with cognitive decline.These results indicate that brain RAGE is an essential factor in the pathogenesis of neurological disorders following acute systemic inflammation.
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The three RAGE forms bind various ligands with similar affinities, including AGEs and amyloid β peptide.
“The three RAGE forms bind various ligands with similar affinities, including multiple advanced glycation end-products (AGEs) and amyloid β peptide31–37.”
From Vascular RAGE transports oxytocin into the brain to elicit its maternal bonding behaviour in mice (2019) · cites this paper as [37]
RAGEs are significantly or markedly expressed in many areas of the brain, such as the cortex, hippocampus, cerebellum, and substantia nigra, during the development of neurodegenerative diseases.
“Similar to AGEs, RAGEs are significantly or markedly expressed in many areas of the brain, such as the cortex, hippocampus, cerebellum, and substantia nigra105–107 during the development of neurodegenerative diseases.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [107]
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Yamamoto, Y., Liang, M., Munesue, S., Deguchi, K., Harashima, A., Furuhara, K., Yuhi, T., Zhong, J., Akther, S., Goto, H., et al. (2019) · Communications Biology · doi:10.1038/s42003-019-0325-6 · Cited by 171 · see citing works
Prantner, D., Nallar, S., & Vogel, S. N. (2020) · The FASEB Journal · doi:10.1096/fj.202002136r · Cited by 92 · see citing works
Gasparotto, J., Ribeiro, C. T., da Rosa-Silva, H. T., Bortolin, R. C., Rabelo, T. K., Peixoto, D. O., Moreira, J. C. F., & Gelain, D. P. (2019) · Molecular Neurobiology · doi:10.1007/s12035-018-1291-6 · Cited by 36 · see citing works
Self-citationRocha, M., Vieira, A., Michels, M., Borges, H., Goulart, A., Fernandes, F., Dominguini, D., Ritter, C., & Dal-Pizzol, F. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2020.104906 · Cited by 20 · see citing works
Self-citationThe brain washing system in sepsis-associated encephalopathy
Chen, T., Hu, J., Liao, Y., Xie, S., & Zhang, L. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03602-4 · Cited by 8 · see citing works
Tang, Y.-F., Duan, Y.-J., Ge, R.-D., Lu, X., Gao, B.-Y., Guo, J.-W., & Jiang, S. (2022) · Journal of Integrative Neuroscience · doi:10.31083/j.jin2201005 · Cited by 5 · see citing works
- Authors
- Gasparotto, J., Girardi, C. S., Somensi, N., Ribeiro, C. T., Moreira, J. C. F., Michels, M., Sonai, B., Rocha, M., Steckert, A. V., Barichello, T., Quevedo, J., Dal-Pizzol, F., & Gelain, D. P.
- Affiliations
- Universidade Federal do Rio Grande do Sul (BR)
- Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (BR)
- Universidade do Extremo Sul Catarinense (BR)
- Corresponding author
- Gelain, Daniel P.
- ORCID
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 293
- Issue
- 1
- Pages
- 226-244
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC5766916
- OpenAlex
- W2767741561
- Cited by
- 120
- References
- 81
- Citations by year
- 2026: 6 · 2025: 16 · 2024: 8 · 2023: 16 · 2022: 18 · 2021: 18 · 2020: 22 · 2019: 9 · 2018: 7
- FWCI
- 8.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (401260/2014–3, 400437/2013–9, 443514/2014–3, 401368/2012–2, 303227/2015–0)
- Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul (16/2551–0000499–4)
- Fundação de Amparo à Pesquisa e Inovação do Estado de Santa Catarina
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- University of Texas Medical School at Houston
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- receptor for advanced glycation end products, RAGE, sepsis, amyloid-beta deposition, tau phosphorylation, cognitive impairment, Akt/mTOR signaling, Iba1, glial fibrillary acidic protein, systemic inflammation, neuroinflammation, neurodegeneration
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Brain, Cognition, Hippocampus, Inflammation, Male, Phosphorylation, Tumor Necrosis Factor-alpha, Signal Transduction, Amyloid beta-Peptides, tau Proteins, Glycation End Products, Advanced, Rats, Wistar, Sepsis, Neurodegenerative Diseases, Rats, Cognitive Dysfunction
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