ArticleJournal of neural transmission (Vienna, Austria : 1996)2010
Association of the RAGE G82S polymorphism with Alzheimer's disease.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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
24 citing papers in PubMed, 51 citations in OpenAlex.
- Current Evidence on the Involvement of RAGE-Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases-An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Article
- Article
- Review
- Diagnostic, Prognostic, and Mechanistic Biomarkers of Diabetes Mellitus-Associated Cognitive Decline.International journal of molecular sciences · 2022Review
- Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.Current drug targets · 2022Article
- Examining the possible causal relationship between lung function, COPD and Alzheimer's disease: a Mendelian randomisation study.BMJ open respiratory research · 2021Article
- G82S RAGE polymorphism influences amyloid-RAGE interactions relevant in Alzheimer's disease pathology.PloS one · 2020Article
- The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.Neurochemistry international · 2019Review
- Pathological Implications of Receptor for Advanced Glycation End-Product (Disease markers · 2019Review
- Biomarkers for cognitive decline in patients with diabetes mellitus: evidence from clinical studies.Oncotarget · 2018Article
- Relationship between RAGE gene polymorphisms and cardiovascular disease prognosis in the Chinese Han population.Molecular genetics and genomics : MGG · 2017Article
- Genetic Association of HLA Gene Variants with MRI Brain Structure in Alzheimer's Disease.Molecular neurobiology · 2017Article
- RAGE and AGEs in Mild Cognitive Impairment of Diabetic Patients: A Cross-Sectional Study.PloS one · 2016Article
- Relationship of advanced glycation end products and their receptor to pelvic organ prolapse.International journal of clinical and experimental pathology · 2015Article
- Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
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- Gly82Ser polymorphism of the receptor for advanced glycation end-product (RAGE) potential high risk in patients with colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- The role of vitamin D in Alzheimer's disease: possible genetic and cell signaling mechanisms.American journal of Alzheimer's disease and other dementias · 2013Review
- RAGE: a new frontier in chronic airways disease.British journal of pharmacology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor for advanced glycation end-products (RAGE) has been implicated in several pathophysiological processes relevant to Alzheimer's disease (AD), including transport and synaptotoxicity of AD-associated amyloid beta (Abeta) peptides. A recent Chinese study (Li et al. in J Neural Transm 117:97-104, 2010) suggested an association between the 82S allele of the functional single nucleotide polymorphism (SNP) G82S (rs2070600) in the RAGE-encoding gene AGER and risk of AD. The present study aimed to investigate associations between AGER, AD diagnosis, cognitive scores and cerebrospinal fluid AD biomarkers in a European cohort of 316 neurochemically verified AD cases and 579 controls. Aside from G82S, three additional tag SNPs were analyzed to cover the common genetic variation in AGER. The 82S allele was associated with increased risk of AD (P (c) = 0.04, OR = 2.0, 95% CI 1.2-3.4). There was no genetic interaction between AGER 82S and APOE epsilon4 in producing increased risk of AD (P = 0.4), and none of the AGER SNPs showed association with Abeta(42), T-tau, P-tau(181) or mini-mental state examination scores. The data speak for a weak, but significant effect of AGER on risk of AD.
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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.