ArticleJournal of Alzheimer's disease : JAD2020
High Dietary Advanced Glycation End Products Impair Mitochondrial and Cognitive Function.
Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- APOE4-AGE axis is linked to mtDNA release and cGAS-STING-mediated neuroinflammation in the aging brain.Free radical biology & medicine · 2026Article
- Advanced glycation end products drive blood-brain barrier lipid dysregulation via RAGE-ABCA1 signaling to promote neurovascular dysfunction in Alzheimer's disease.Molecular psychiatry · 2026Article
- Cutaneous Aging in Skin of Color: A Narrative Review.American journal of clinical dermatology · 2026Review
- α/Sulfonyl-γ-AApeptide foldamers mitigate Alzheimer's disease pathology by stabilizing transient helical domains in Aβ.Nature communications · 2026Article
- Glycation at the Crossroads of Disease Pathogenesis: Mechanistic Insights and Therapeutic Frontiers.Diseases (Basel, Switzerland) · 2026Review
- APOE4 impairs Nrf2-PINK1/Parkin-dependent mitochondrial clearance through disrupted antioxidant and mitophagy signaling.Free radical biology & medicine · 2026Article
- Consumption of processed foods impairs memory function through dietary advanced glycation end-products.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial oxidative stress promotes the accumulation of advanced glycation end products.PloS one · 2026Article
- Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Impact of Diverse Dietary Patterns on Cognitive Health: Cumulative Evidence from Prospective Cohort Studies.Nutrients · 2025Review
- Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.Antioxidants (Basel, Switzerland) · 2025Review
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Synaptic mitochondria glycation contributes to mitochondrial stress and cognitive dysfunction.Brain : a journal of neurology · 2025Article
- Dietary methionine supplementation improves cognitive dysfunction associated with transsulfuration pathway upregulation in subacute aging mice.NPJ science of food · 2024Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- Associations of Glucose Metabolism Status with Brain Macrostructure and Microstructure: Findings from the UK Biobank.The Journal of clinical endocrinology and metabolism · 2023Article
- Homeostasis of carbohydrates and reactive oxygen species is critically changed in the brain of middle-aged mice: Molecular mechanisms and functional reasons.BBA advances · 2023Article
- Receptors for Advanced Glycation End Products (RAGE): Promising Targets Aiming at the Treatment of Neurodegenerative Conditions.Current neuropharmacology · 2023Review
- The Influence of Cationic Nitrosyl Iron Complex with Penicillamine Ligands on Model Membranes, Membrane-Bound Enzymes and Lipid Peroxidation.Membranes · 2022Article
- The Effects of Dietary Advanced Glycation End-Products on Neurocognitive and Mental Disorders.Nutrients · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAdvanced glycation end products (AGEs) are an important risk factor for the development of cognitive decline in aging and late-onset neurodegenerative diseases including Alzheimer's disease. However, whether and how dietary AGEs exacerbate cognitive impairment and brain mitochondrial dysfunction in the aging process remains largely unknown.
objectiveWe investigated the direct effects of dietary AGEs on AGE adducts accumulation, mitochondrial function, and cognitive performance in mice.
methodsMice were fed the AGE+ diet or AGE- diet. We examined levels of AGE adducts in serum and cerebral cortexes by immunodetection and immunohistochemistry, determined levels of reactive oxygen species by biochemical analysis, detected enzyme activity associated with mitochondrial respiratory chain complexes I & IV and ATP levels, and assessed learning and memory ability by Morris Water Maze and nesting behavior.
resultsLevels of AGE adducts (MG-H1 and CEL) were robustly increased in the serum and brain of AGE+ diet fed mice compared to the AGE- group. Furthermore, greatly elevated levels of reactive oxygen species, decreased activities of mitochondrial respiratory chain complexes I & IV, reduced ATP levels, and impaired learning and memory were evident in AGE+ diet fed mice compared to the AGE- group.
conclusionThese results indicate that dietary AGEs are important sources of AGE accumulation in vivo, resulting in mitochondrial dysfunction, impairment of energy metabolism, and subsequent cognitive impairment. Thus, reducing AGEs intake to lower accumulation of AGEs could hold therapeutic potential for the prevention and treatment of AGEs-induced mitochondrial dysfunction linked to cognitive decline.
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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.