ReviewJournal of molecular neuroscience : MN2024
Advanced Glycation End Products in Neurodegenerative Diseases.
Review in Journal of molecular neuroscience : MN, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed.
- Behavioral, neuroanatomic, and neuroinflammatory characteristics of metabolic syndrome in cafeteria diet-induced obese male rats.Metabolic brain disease · 2026Article
- Monoclonal Antibody-Based ELISA Quantification of Serum Methylglyoxal-Derived Hydroimidazolone-1.Diagnostics (Basel, Switzerland) · 2026Article
- Label-Free Evaluation of Advanced Glycation End Products by a Comprehensive Biophysical Analysis.Analytical chemistry · 2026Article
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Identification of senescence-related genes in Parkinson's disease reveals candidate therapeutic targets and pathological processes.Animal models and experimental medicine · 2026Article
- Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences.Neurology. Clinical practice · 2026Review
- Exploring the therapeutic potential of the gut microbiota metabolite 3‑indolepropionic acid in parkinson's disease: a network pharmacology, molecular docking and cell viability study.Metabolic brain disease · 2026Article
- Deciphering the Multi-Target Therapeutic Mechanisms of Traditional Chinese Medicine Against Alzheimer's Disease: A Network Pharmacology Perspective.Drug design, development and therapy · 2026Review
- Algae-Derived C-Phycocyanin Mitigates AGE-RAGE-Induced ER Stress and Mitochondrial Apoptosis: Implications for Diabetes-Associated Neurodegeneration.International journal of molecular sciences · 2025Article
- α-Methyltryptophan mitigates cognitive impairment in db/db mice: involvement of gut-brain metabolic remodeling.Nutrition & metabolism · 2025Article
- Associations of dietary advanced glycation end products and the risk of depression and anxiety.European journal of nutrition · 2025Article
- Type 2 diabetes and depression via microvascular dysfunction, neurodegeneration, inflammation, advanced glycation end products (AGEs), and arterial stiffness.Diabetes, obesity & metabolism · 2025Article
- Sex-specific differences of advanced glycation end products in diabetes.Nutrition & diabetes · 2025Review
- Unraveling the Role of Functional Amyloids and Amyloid Peptides in Disease Detection.Protein and peptide letters · 2025Review
- Acetaldehyde and methylglyoxal: comparative analysis of toxic electronic cigarette degradation products in 3D and 2D exposure systems using human bronchial epithelial models.Frontiers in toxicology · 2025Article
- The Remodeling of Mitochondrial-Endoplasmic Reticulum Contacts by Omega-3 Fatty Acids Mitigates Dietary Advanced Glycation End Product-Driven Sertoli Cell Senescence and Oligoasthenozoospermia.International journal of biological sciences · 2025Article
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- Glycated Hemoglobin and Cardiovascular Disease in Patients Without Diabetes.Journal of clinical medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs) have attracted interest as therapeutic targets for neurodegenerative diseases. AGEs facilitate the onset and progression of various neurogenerative disorders due to their ability to promote cross-linking and aggregation of proteins. Further, the interaction between AGEs and receptor for AGEs (RAGE) activates neuroinflammatory, oxidative stress and excitotoxicity processes that contribute to neuronal cell death. Various therapeutic efforts have targeted lowering the production of AGEs, inhibiting RAGE or inhibiting some of the processes of the AGE-RAGE axis as potential treatments for these disorders. Whereas effective treatments for many neurodegenerative disorders remain elusive, such efforts offer promise to slow the progression of diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD).
Indexed as
Identifiers
39653979What 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.