Evidence map›Paper›PMID 35052650›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy.

Ryszard Pluta, Jacek Kiś, Sławomir Januszewski, Mirosław Jabłoński, Stanisław J Czuczwar

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. [Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Article
  3. Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. International journal of molecular sciences · 2024
    Article
  10. ACS omega · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

5 authors at 3 institutions in 1 country.

Ryszard PlutaLaboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, Poland.ORCID 0000-0003-0764-1356
Jacek KiśDepartment of Urology, 1st Military Clinical Hospital with the Outpatient Clinic, Al. Racławickie 23, 20-049 Lublin, Poland.
Sławomir JanuszewskiLaboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, Poland.
Mirosław JabłońskiDepartment of Rehabilitation and Orthopedics, Medical University of Lublin, Jaczewskiego 8 Str., 20-090 Lublin, Poland.
Stanisław J CzuczwarDepartment of Pathophysiology, Medical University of Lublin, Jaczewskiego 8b Str., 20-090 Lublin, Poland.
Medical University of Lublin · PLPolish Academy of Sciences · PL1 Military Clinical Hospital with Outpatient Clinic · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer's disease proteinopathy.

Indexed as

amyloidbrain ischemiaelastin-derived peptidesfree radicalhormesisoxidative stressproteinopathyreactive nitrogen speciesreactive oxygen speciestau proteinvitagene

Identifiers

PMID35052650
PMCPMC8772936
OpenAlexW4205236128

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.