ReviewCureus2024
Advanced Glycation End Products-Induced Alzheimer's Disease and Its Novel Therapeutic Approaches: A Comprehensive Review.
Review in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- In vitro and in silico studies and a systematic literature review of antiglycation properties of amlodipine.Scientific reports · 2025Pooled it
- Microvascular damage in diabetic nephropathy and the subsequent risk of Alzheimer's disease: a systematic review.Annals of medicine and surgery (2012) · 2026Article
- Caveolin-1 at the Crossroads of Diabetes and Alzheimer's Disease: New Mechanisms, Biomarkers, and Therapeutic Opportunities.Biomedicines · 2026Review
- Oxidative Stress in Alzheimer's Disease: Can Dietary Interventions Provide Neuroprotection?Nutrients · 2026Review
- Reduction of glycation stress as a geroscience intervention: protocol for a pilot RCT in postmenopausal women.npj aging · 2026Article
- Glycation at the Crossroads of Disease Pathogenesis: Mechanistic Insights and Therapeutic Frontiers.Diseases (Basel, Switzerland) · 2026Review
- Bridging the Gut Microbiota and the Brain, Kidney, and Cardiovascular Health: The Role of Probiotics.Probiotics and antimicrobial proteins · 2026Review
- β-Hydroxybutyrate attenuates glycation-induced structural destabilization and amyloidogenic aggregation in human serum albumin.Biochemistry and biophysics reports · 2026Article
- FA-2-b-β modulates HMGB1/NF-κB/NLRP3 signaling to alleviate neuroinflammation in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- The AGE-RAGE Pathway in Endometriosis: A Focused Mechanistic Review and Structured Evidence Map.International journal of molecular sciences · 2026Review
- Apelin-13 confers Neuropeptide Y-mediated neuroprotection and preserves learning and allocentric memory in D-glutamic acid-induced excitotoxicity in rats.Molecular neurobiology · 2026Article
- Pollutants regulate changes in pathological markers of neurodegenerative diseases: a new perspective in environmental toxicology.Frontiers in toxicology · 2026Review
- Glycation in Alzheimer's Disease and Type 2 Diabetes: The Prospect of Dual Drug Approaches for Therapeutic Interventions.Molecular neurobiology · 2025Review
- Current Developments in Analytical Methods for Advanced Glycation End Products in Foods.Molecules (Basel, Switzerland) · 2025Review
- Article
- Oxidative Stress, Advanced Glycation End Products (AGEs), and Neurodegeneration in Alzheimer's Disease: A Metabolic Perspective.Antioxidants (Basel, Switzerland) · 2025Review
- Glucose Extremes and Cognitive Function: A Review of the Neurological Impacts of Hypoglycemia and Hyperglycemia in Type 1 Diabetes.Diabetes spectrum : a publication of the American Diabetes Association · 2025Article
- Immune Reactivity to Raw and Processed Foods and Their Possible Contributions to Autoimmunity.Foods (Basel, Switzerland) · 2025Review
- Glycation of Proteins and Its End Products: From Initiation to Natural Product-Based Therapeutic Preventions.ACS pharmacology & translational science · 2025Review
- Cognitive decline in older adults with type 2 diabetes: Unraveling site-specific glycoproteomic alterations.PloS one · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs) accumulate in the brain, leading to neurodegenerative conditions such as Alzheimer's disease (AD). The pathophysiology of AD is influenced by receptors for AGEs and toll-like receptor 4 (TLR4). Protein glycation results in irreversible AGEs through a complicated series of reactions involving the formation of Schiff's base, the Amadori reaction, followed by the Maillard reaction, which causes abnormal brain glucose metabolism, oxidative stress, malfunctioning mitochondria, plaque deposition, and neuronal death. Amyloid plaque and other stimuli activate macrophages, which are crucial immune cells in AD development, triggering the production of inflammatory molecules and contributing to the disease's pathogenesis. The risk of AD is doubled by risk factors for atherosclerosis, dementia, advanced age, and type 2 diabetic mellitus (DM). As individuals age, the prevalence of neurological illnesses such as AD increases due to a decrease in glyoxalase levels and an increase in AGE accumulation. Insulin's role in proteostasis influences hallmarks of AD-like tau phosphorylation and amyloid β peptide clearance, affecting lipid metabolism, inflammation, vasoreactivity, and vascular function. The high-mobility group box 1 (HMGB1) protein, a key initiator and activator of a neuroinflammatory response, has been linked to the development of neurodegenerative diseases such as AD. The TLR4 inhibitor was found to improve memory and learning impairment and decrease Aβ build-up. Therapeutic research into anti-glycation agents, receptor for advanced glycation end products (RAGE) inhibitors, and AGE breakers offers hope for intervention strategies. Dietary and lifestyle modifications can also slow AD progression. Newer therapeutic approaches targeting AGE-related pathways are needed.
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What OpenQuestion holds
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.