Evidence map›Paper›PMID 34571862›Full record

ReviewCells2021

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer's Disease Type.

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

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Loss of cerebral autoregulation drives abnormal perfusion patterns after stroke.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. International journal of molecular sciences · 2024
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  9. ACS omega · 2024
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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

4 authors at 2 institutions in 1 country.

Ryszard PlutaLaboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Str. Pawińskiego, 02-106 Warsaw, Poland.ORCID 0000-0003-0764-1356
Stanisław J CzuczwarDepartment of Pathophysiology, Medical University of Lublin, 8b Str. Jaczewskiego, 20-090 Lublin, Poland.ORCID 0000-0003-2879-9945
Sławomir JanuszewskiLaboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Str. Pawińskiego, 02-106 Warsaw, Poland.
Mirosław JabłońskiDepartment of Rehabilitation and Orthopedics, Medical University of Lublin, 8 Str. Jaczewskiego, 20-090 Lublin, Poland.
Medical University of Lublin · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified tau protein in a manner typical of Alzheimer's disease neuropathology. Pathological changes in the tau protein, at the gene and protein level due to cerebral ischemia, can lead to the development of Alzheimer's disease-type neuropathology and dementia. Some studies have shown increased tau protein staining and gene expression in neurons following ischemia-reperfusion brain injury. Recent studies have found the tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity, neuroinflammation, blood-brain barrier permeability, mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the tau protein in the brain. The tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following ischemia. The data indicate that an episode of cerebral ischemia activates the damage and death of neurons in the hippocampus in a tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following ischemia. In this review, we update our understanding of proteomic and genomic changes in the tau protein in post-ischemic brain injury and present the relationship between the modified tau protein and post-ischemic neuropathology and present a positive correlation between the modified tau protein and a post-ischemic neuropathology that has characteristics of Alzheimer's disease-type neurodegeneration.

Indexed as

Alzheimer DiseaseAnimalsBlood-Brain BarrierBrain IschemiaHumansNeuronsReperfusion Injurytau Proteinstau Proteinsapoptosisautophagybrain ischemiadementiaexcitotoxicitygenhippocampusmitochondrial dysfunctionneurodegenerationneurofibrillary tanglesneuroinflammationneuronal deathoxidative stresstau protein

Identifiers

PMID34571862
PMCPMC8465797
OpenAlexW3197345443

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.