Evidence map›Paper›PMID 34884729›Full record

ReviewInternational journal of molecular sciences2021

Impact of Oxidative DNA Damage and the Role of DNA Glycosylases in Neurological Dysfunction.

Mirta Mittelstedt Leal de Sousa, Jing Ye, Luisa Luna, Gunn Hildrestrand, Karine Bjørås, Katja Scheffler, Magnar Bjørås

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Mirta Mittelstedt Leal de SousaDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7028 Trondheim, Norway.ORCID 0000-0002-4559-2551
Jing YeDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7028 Trondheim, Norway.
Luisa LunaDepartment of Microbiology, Oslo University Hospital, University of Oslo, Rikshospitalet, 0424 Oslo, Norway.
Gunn HildrestrandDepartment of Microbiology, Oslo University Hospital, University of Oslo, Rikshospitalet, 0424 Oslo, Norway.ORCID 0000-0003-3160-7203
Karine BjøråsDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7028 Trondheim, Norway.
Katja SchefflerDepartment of Neurology, St. Olavs Hospital, 7006 Trondheim, Norway.ORCID 0000-0002-1734-7807
Magnar BjøråsDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7028 Trondheim, Norway.ORCID 0000-0001-8759-1170
Norwegian University of Science and Technology · NOOslo University Hospital · NO

Funding

The Research Council of Norway 90421400
6 · The paper itself

Abstract

The human brain requires a high rate of oxygen consumption to perform intense metabolic activities, accounting for 20% of total body oxygen consumption. This high oxygen uptake results in the generation of free radicals, including reactive oxygen species (ROS), which, at physiological levels, are beneficial to the proper functioning of fundamental cellular processes. At supraphysiological levels, however, ROS and associated lesions cause detrimental effects in brain cells, commonly observed in several neurodegenerative disorders. In this review, we focus on the impact of oxidative DNA base lesions and the role of DNA glycosylase enzymes repairing these lesions on brain function and disease. Furthermore, we discuss the role of DNA base oxidation as an epigenetic mechanism involved in brain diseases, as well as potential roles of DNA glycosylases in different epigenetic contexts. We provide a detailed overview of the impact of DNA glycosylases on brain metabolism, cognition, inflammation, tissue loss and regeneration, and age-related neurodegenerative diseases based on evidence collected from animal and human models lacking these enzymes, as well as post-mortem studies on patients with neurological disorders.

Indexed as

DNA RepairOxidative StressAnimalsBrainBrain InjuriesDNA GlycosylasesEpigenesis, GeneticHumansNeurodegenerative DiseasesRegenerationDNA GlycosylasesDNA glycosylasesDNA repairepigenetic markersneurological disordersoxidative DNA lesions

Identifiers

PMID34884729
PMCPMC8657561
OpenAlexW3215998853

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.