ArticleAntioxidants & redox signaling2013
Trientine reduces BACE1 activity and mitigates amyloidosis via the AGE/RAGE/NF-κB pathway in a transgenic mouse model of Alzheimer's disease.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- [Gandou Bushen decoction ameliorates ovarian injury in murine hepatolenticular degeneration via the AGE/RAGE/NF-κB signaling pathway].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Article
- Plasma Glial Fibrillary Acidic Protein Correlates With Brain Metal Burden in Wilson's Disease.Annals of clinical and translational neurology · 2025Article
- Gut microbial-derived indole-3-propionate improves cognitive function in Alzheimer's disease.Science advances · 2025Article
- Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.Signal transduction and targeted therapy · 2025Review
- A Novel RAGE Modulator Induces Soluble RAGE to Reduce BACE1 Expression in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Recent Advances in Targeting Transition Metals (Copper, Iron, and Zinc) in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Copper homeostasis and cuproptosis in central nervous system diseases.Cell death & disease · 2024Review
- Targeting Biometals in Alzheimer's Disease with Metal Chelating Agents Including Coumarin Derivatives.CNS drugs · 2024Review
- Advanced glycation end product-modified low-density lipoprotein promotes pro-osteogenic reprogramming via RAGE/NF-κB pathway and exaggerates aortic valve calcification in hamsters.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- Drug repurposing for neurodegenerative diseases using Zebrafish behavioral profiles.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Metabolic Disorder Therapeutics and their Effects on Memory.CNS & neurological disorders drug targets · 2024Review
- Using Small Molecules for Targeting Heavy Metals in Neurotoxicity and Neuroinflammation.Methods in molecular biology (Clifton, N.J.) · 2024Article
- A Novel Cu(II)-Binding Peptide Identified by Phage Display Inhibits CuInternational journal of molecular sciences · 2021Article
- Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer's disease.IBRO neuroscience reports · 2021Article
- Preventive and Therapeutic Strategies in Alzheimer's Disease: Focus on Oxidative Stress, Redox Metals, and Ferroptosis.Antioxidants & redox signaling · 2021Review
- Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury.Experimental & molecular medicine · 2021Review
- Autophagy and Glycative Stress: A Bittersweet Relationship in Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThere is mounting evidence that the transition metal copper may play an important role in the pathophysiology of Alzheimer's disease (AD). Triethylene tetramine dihydrochloride (trientine), a CuII-selective chelator, is a commonly used treatment for Wilson's disease to decrease accumulated copper, and thereby decreases oxidative stress. In the present study, we evaluated the effects of a 3-month treatment course of trientine (Trien) on amyloidosis in 7-month-old β-amyloid (Aβ) precursor protein and presenilin-1 (APP/PS1) double transgenic (Tg) AD model mice.
resultsWe observed that Trien reduced the level of advanced glycation end products (AGEs), and decreased Aβ deposition and synapse loss in brain of APP/PS1 mice. Importantly, we found that Trien blocked the receptor for AGEs (RAGE), downregulated β-site APP cleaving enzyme 1 (BACE1), inhibited amyloidogenic APP cleavage, and subsequently reduced Aβ levels. In vitro, in SH-SY5Y cells overexpressing Swedish mutant APP, Trien-mediated downregulation of BACE1 occurred via inhibition of the NF-κB signaling pathway. INNOVATION: In this study, we demonstrated for the first time that Trien inhibited amyloidogenic pathway including targeting the downregulation of RAGE and NF-κB.
conclusionTrien might mitigate amyloidosis in AD by inhibiting the RAGE/NF-κB/BACE1 pathway. Our study demonstrates that Trien may be a viable therapeutic strategy for the intervention and treatment of AD and other AD-like pathologies.
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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.