Evidence map›Paper›PMID 34573082›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases.

Ioannis Gkekas, Anna Gioran, Marina Kleopatra Boziki, Nikolaos Grigoriadis, Niki Chondrogianni, Spyros Petrakis

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Erinacine A-EnrichedAntioxidants (Basel, Switzerland) · 2024
    Article
  3. Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. The flavonoid luteolin reduces mutant huntingtin aggregation and cytotoxicity in huntingtin-mutated neuroblastoma cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  10. Article
  11. Review
  12. ReducedAntioxidants (Basel, Switzerland) · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Oncogenic Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
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

6 authors at 3 institutions in 1 country.

Ioannis GkekasInstitute of Applied Biosciences/Centre for Research and Technology Hellas, 57001 Thessaloniki, Greece.
Anna GioranInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.ORCID 0000-0003-3276-4702
Marina Kleopatra Boziki2nd Neurological Department, AHEPA University General Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece.ORCID 0000-0002-6601-5163
Nikolaos Grigoriadis2nd Neurological Department, AHEPA University General Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece.
Niki ChondrogianniInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.
Spyros PetrakisInstitute of Applied Biosciences/Centre for Research and Technology Hellas, 57001 Thessaloniki, Greece.ORCID 0000-0001-9094-3480
Aristotle University of Thessaloniki · GRCentre for Research and Technology Hellas · GRNational Hellenic Research Foundation · GR

Funding

Hellenic Foundation for Research and Innovation 122
6 · The paper itself

Abstract

Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which are associated with selective neuronal degeneration. Several lines of evidence indicate that these mutant proteins are associated with oxidative stress, proteasome impairment and microglia activation. These events may correlate with the induction of inflammation in the nervous system and disease progression. Here, we review the effect of polyQ-induced oxidative stress in cellular and animal models of polyQ diseases. Furthermore, we discuss the interplay between oxidative stress, neurodegeneration and neuroinflammation using as an example the well-known neuroinflammatory disease, Multiple Sclerosis. Finally, we review some of the pharmaceutical interventions which may delay the onset and progression of polyQ disorders by targeting disease-associated mechanisms.

Indexed as

microglia activationneurodegenerationneuroinflammationoxidative stresspolyglutamineproteasome impairment

Identifiers

PMID34573082
PMCPMC8471619
OpenAlexW3201075689

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.