Evidence map›Paper›PMID 27392670›Full record

ReviewAntioxidants & redox signaling2016

The Proteasome and Oxidative Stress in Alzheimer's Disease.

Vicent Bonet-Costa, Laura Corrales-Diaz Pomatto, Kelvin J A Davies

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
–field-weighted citation impact
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

57 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Ubiquitin-proteasome system in the different stages of dominantly inherited Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Understanding mechanisms of antioxidant action in health and disease.Nature reviews. Molecular cell biology · 2024
    Review
  17. Review
  18. Review
  19. Cross-Platform Synaptic Network Analysis of Human Entorhinal Cortex Identifies TWF2 as a Modulator of Dendritic Spine Length.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  20. 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

3 authors.

Vicent Bonet-CostaLeonard Davis School of Gerontology, Ethel Percy Andrus Gerontology Center, The Division of Molecular and Computational Biology, Department of Biological Sciences, Dornsife College of Letters, Arts, and Sciences, The University of Southern California , Los Angeles, California.
Laura Corrales-Diaz PomattoLeonard Davis School of Gerontology, Ethel Percy Andrus Gerontology Center, The Division of Molecular and Computational Biology, Department of Biological Sciences, Dornsife College of Letters, Arts, and Sciences, The University of Southern California , Los Angeles, California.
Kelvin J A DaviesLeonard Davis School of Gerontology, Ethel Percy Andrus Gerontology Center, The Division of Molecular and Computational Biology, Department of Biological Sciences, Dornsife College of Letters, Arts, and Sciences, The University of Southern California , Los Angeles, California.

Funding

OXYGEN RADICAL TOXICITY AND RED CELL PROTEIN DEGRADATIONR01ES003598 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DAVIES, KELVIN J. A. · 1988 to 2017
$5.7M
USC Geroscience Training in the Biology of AgingT32AG052374 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Sean P CURRAN · 2016 to 2026
$5.3M
NIA NIH HHS T32 AG052374NIEHS NIH HHS R01 ES003598
6 · The paper itself

Abstract

significanceAlzheimer's disease is a neurodegenerative disorder that is projected to exceed more than 100 million cases worldwide by 2050. Aging is considered the primary risk factor for some 90% of Alzheimer's cases but a significant 10% of patients suffer from aggressive, early-onset forms of the disease. There is currently no effective Alzheimer's treatment and this, coupled with a growing aging population, highlights the necessity to understand the mechanism(s) of disease initiation and propagation. A major hallmark of Alzheimer's disease pathology is the accumulation of amyloid-β (Aβ) aggregates (an early marker of Alzheimer's disease), and neurofibrillary tangles, comprising the hyper-phosphorylated microtubule-associated protein Tau. Recent Advances: Protein oxidation is frequently invoked as a potential factor in the progression of Alzheimer's disease; however, whether it is a cause or a consequence of the pathology is still being debated. The Proteasome complex is a major regulator of intracellular protein quality control and an essential proteolytic enzyme for the processing of both Aβ and Tau. Recent studies have indicated that both protein oxidation and excessive phosphorylation may limit Proteasomal processing of Aβ and Tau in Alzheimer's disease. CRITICAL ISSUES: Thus, the Proteasome may be a key factor in understanding the development of Alzheimer's disease pathology; however, its significance is still very much under investigation. FUTURE DIRECTIONS: Discovering how the proteasome is affected, regulated, or dysregulated in Alzheimer's disease could be a valuable tool in the efforts to understand and, ultimately, eradicate the disease. Antioxid. Redox Signal. 25, 886-901.

Indexed as

Oxidative StressAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansMitochondriaOxidation-ReductionPhosphorylationProtease LaProteasome Endopeptidase ComplexProteolysistau ProteinsAmyloid beta-PeptidesProtease LaProteasome Endopeptidase Complextau ProteinsAlzheimer's diseasedementiaoxidative stressproteasomeprotein oxidationproteolysis

Identifiers

PMID27392670
PMCPMC5124752

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.