ArticleCell death & disease2014
Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 36 citations in OpenAlex.
- SGLT2 Inhibitors in Alzheimer's Disease: Biochemical Insights and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Mitochondrial oxidative stress promotes the accumulation of advanced glycation end products.PloS one · 2026Article
- Targeting the RAGE-RIPK1 binding site attenuates diabetes-associated cognitive deficits.Journal of neuroinflammation · 2025Article
- Association Between the Gut Microbiota and Alzheimer's Disease: An Update on Signaling Pathways and Translational Therapeutics.Molecular neurobiology · 2025Review
- Synaptic mitochondria glycation contributes to mitochondrial stress and cognitive dysfunction.Brain : a journal of neurology · 2025Article
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- Deletion of RAGE fails to prevent hepatosteatosis in obese mice due to impairment of other AGEs receptors and detoxifying systems.Scientific reports · 2021Article
- Age-dependent accumulation of dicarbonyls and advanced glycation endproducts (AGEs) associates with mitochondrial stress.Free radical biology & medicine · 2021Article
- Review
- High Dietary Advanced Glycation End Products Impair Mitochondrial and Cognitive Function.Journal of Alzheimer's disease : JAD · 2020Article
- Systemic Inflammation Changes the Site of RAGE Expression from Endothelial Cells to Neurons in Different Brain Areas.Molecular neurobiology · 2019Article
- High glucose-induced complement component 3 up-regulation via RAGE-p38MAPK-NF-κB signalling in astrocytes: In vivo and in vitro studies.Journal of cellular and molecular medicine · 2018Article
- Overexpression of endophilin A1 exacerbates synaptic alterations in a mouse model of Alzheimer's disease.Nature communications · 2018Article
- RAGE mediates Aβ accumulation in a mouse model of Alzheimer's disease via modulation of β- and γ-secretase activity.Human molecular genetics · 2018Article
- Targeted inhibition of RAGE in substantia nigra of rats blocks 6-OHDA-induced dopaminergic denervation.Scientific reports · 2017Article
- Glycation & the RAGE axis: targeting signal transduction through DIAPH1.Expert review of proteomics · 2017Review
- Mitochondrial Perturbation in Alzheimer's Disease and Diabetes.Progress in molecular biology and translational science · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Synaptic dysfunction and degeneration is an early pathological feature of aging and age-related diseases, including Alzheimer's disease (AD). Aging is associated with increased generation and deposition of advanced glycation endproducts (AGEs), resulting from nonenzymatic glycation (or oxidation) proteins and lipids. AGE formation is accelerated in diabetes and AD-affected brain, contributing to cellular perturbation. The extent of AGEs' involvement, if at all, in alterations in synaptic structure and function is currently unknown. Here we analyze the contribution of neuronal receptor of AGEs (RAGE) signaling to AGE-mediated synaptic injury using novel transgenic neuronal RAGE knockout mice specifically targeted to the forebrain and transgenic mice expressing neuronal dominant-negative RAGE (DN-RAGE). Addition of AGEs to brain slices impaired hippocampal long-term potentiation (LTP). Similarly, treatment of hippocampal neurons with AGEs significantly decreases synaptic density. Such detrimental effects are largely reversed by genetic RAGE depletion. Notably, brain slices from mice with neuronal RAGE deficiency or DN-RAGE are resistant to AGE-induced LTP deficit. Further, RAGE deficiency or DN-RAGE blocks AGE-induced activation of p38 signaling. Taken together, these data show that neuronal RAGE functions as a signal transducer for AGE-induced synaptic dysfunction, thereby providing new insights into a mechanism by which the AGEs-RAGE-dependent signaling cascade contributes to synaptic injury via the p38 MAP kinase signal transduction pathway. Thus, RAGE blockade may be a target for development of interventions aimed at preventing the progression of cognitive decline in aging and age-related neurodegenerative diseases.
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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.