Evidence map›Paper›PMID 31079281›Full record

ReviewMolecular and cellular biochemistry2019

AGE-RAGE stress: a changing landscape in pathology and treatment of Alzheimer's disease.

Kailash Prasad

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
9.0field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Are Advanced Glycation End Products in Skin Associated with Vascular Dysfunction Markers? A Meta-Analysis.International journal of environmental research and public health · 2020
    Pooled it
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Modulating the RAGE-Induced Inflammatory Response: Peptoids as RAGE Antagonists.Chembiochem : a European journal of chemical biology · 2023
    Article
  16. Article
  17. Spinosin protects Neuro-2a/APP695 cells from oxidative stress damage by inactivating p38.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023
    Article
  18. Review
  19. Article
  20. S100B, Actor and Biomarker of Mild Traumatic Brain Injury.International journal of molecular sciences · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kailash PrasadDepartment of Physiology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada. k.prasad@usask.ca.ORCID http://orcid.org/0000-0001-5935-7774
University of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous hypotheses including amyloid cascade, cholinergic, and oxidative have been proposed for pathogenesis of Alzheimer's disease (AD). The data suggest that advanced glycation end products (AGEs) and its receptor RAGE (receptor for AGE) are involved in the pathogenesis of AD. AGE-RAGE stress, defined as a balance between stressors (AGE, RAGE) and anti-stressors (sRAGE, AGE degraders) in favor of stressors, has been implicated in pathogenesis of diseases. AGE and its interaction with RAGE-mediated increase in the reactive oxygen species (ROS) damage brain because of its increased vulnerability to ROS. AGE and ROS increase the synthesis of amyloid β (Aβ) leading to deposition of Aβ and phosphorylation of tau, culminating in formation of plaques and neurofibrillary tangles. ROS increase the synthesis of Aβ, high-mobility group box 1(HMGB1), and S100 that interacts with RAGE to produce additional ROS resulting in enhancement of AD pathology. Elevation of ROS precedes the Aβ plaques formation. Because of involvement of AGE and RAGE in AD pathology, the treatment should be targeted at lowering AGE levels through reduction in consumption and formation of AGE, and lowering expression of RAGE, blocking of RAGE ligand binding, increasing levels of soluble RAGE (sRAGE), and use of antioxidants. The above treatment aspect of AD is lacking. In conclusion, AGE-RAGE stress initiates, and Aβ, HMGB1, and S100 enhance the progression of AD. Reduction of levels of AGE and RAGE, elevation of sRAGE, and antioxidants would be beneficial therapeutic modalities in the prevention, regression, and slowing of progression of AD.

Indexed as

Oxidative StressAlzheimer DiseaseAmyloid beta-PeptidesBrainGlycation End Products, AdvancedHMGB1 ProteinHumansReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsS100 ProteinsAGER protein, humanAmyloid beta-PeptidesGlycation End Products, AdvancedHMGB1 ProteinHMGB1 protein, humanReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsS100 ProteinsAdvanced glycation end products (AGE)AGE–RAGE stressAlzheimer’s disease (AD)Manipulation of AGE–RAGE axis in treatment of ADPathogenesis of ADReceptor of AGE (RAGE)

Identifiers

PMID31079281
OpenAlexW2943963095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.