Evidence map›Paper›PMID 27234294›Full record

ArticleMolecular brain2016

Altered DNA base excision repair profile in brain tissue and blood in Alzheimer's disease.

Meryl S Lillenes, Alberto Rabano, Mari Støen, Tahira Riaz, Dorna Misaghian, Linda Møllersen, Ying Esbensen, Clara-Cecilie Günther, Per Selnes, Vidar T V Stenset and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 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

12 authors at 5 institutions in 2 countries.

Meryl S LillenesDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Alberto RabanoFundación Centro Investigación Enfermedades Neurológicas (CIEN), Madrid, Spain.
Mari StøenDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Tahira RiazDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Dorna MisaghianDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Linda MøllersenDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Ying EsbensenDepartment of Clinical Molecular Biology and Laboratory Sciences (EpiGen), Division of Medicine, Akershus University Hospital and University of Oslo, Lørenskog, Norway.
Clara-Cecilie GüntherNorwegian Computing Center, Oslo, Norway.
Per SelnesDepartment of Neurology, Faculty Division, Akershus University Hospital, University of Oslo, Lørenskog, Norway.
Vidar T V StensetDepartment of Neurology, Faculty Division, Akershus University Hospital, University of Oslo, Lørenskog, Norway.
Tormod FladbyDepartment of Neurology, Faculty Division, Akershus University Hospital, University of Oslo, Lørenskog, Norway.
Tone TønjumDepartment of Microbiology, Oslo University Hospital, Oslo, Norway. tone.tonjum@medisin.uio.no.
Oslo University Hospital · NOAkershus University Hospital · NOCentro de Estudios AndalucesNorwegian Computing Center · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a progressive, multifactorial neurodegenerative disorder that is the main cause of dementia globally. AD is associated with increased oxidative stress, resulting from imbalance in production and clearance of reactive oxygen species (ROS). ROS can damage DNA and other macromolecules, leading to genome instability and disrupted cellular functions. Base excision repair (BER) plays a major role in repairing oxidative DNA lesions. Here, we compared the expression of BER components APE1, OGG1, PARP1 and Polβ in blood and postmortem brain tissue from patients with AD, mild cognitive impairment (MCI) and healthy controls (HC).

resultsBER mRNA levels were correlated to clinical signs and cerebrospinal fluid biomarkers for AD. Notably, the expression of BER genes was higher in brain tissue than in blood samples. Polβ mRNA and protein levels were significantly higher in the cerebellum than in the other brain regions, more so in AD patients than in HC. Blood mRNA levels of OGG1 was low and PARP1 high in MCI and AD.

conclusionsThese findings reflect the oxidative stress-generating energy-consumption in the brain and the importance of BER in repairing these damage events. The data suggest that alteration in BER gene expression is an event preceding AD. The results link DNA repair in brain and blood to the etiology of AD at the molecular level and can potentially serve in establishing novel biomarkers, particularly in the AD prodromal phase.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBiomarkersBrainCase-Control StudiesDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA Polymerase betaDNA RepairFemaleGene Expression RegulationHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedAPEX1 protein, humanBiomarkersDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA Polymerase betaoxoguanine glycosylase 1, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1RNA, MessengerAlzheimer’s diseaseAPE1Base excision repairBrain tissueDNA glycosylase OGG1DNA polymerase PolβDNA repairPARP1

Identifiers

PMID27234294
PMCPMC4884418
OpenAlexW2406870746

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.