Evidence map›Paper›PMID 24936870›Full record

ArticlePloS one2014

Repair of oxidative DNA damage, cell-cycle regulation and neuronal death may influence the clinical manifestation of Alzheimer's disease.

Aderbal R T Silva, Ana Cecília Feio Santos, Jose M Farfel, Lea T Grinberg, Renata E L Ferretti, Antonio Hugo Jose Froes Marques Campos, Isabela Werneck Cunha, Maria Dirlei Begnami, Rafael M Rocha, Dirce M Carraro and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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  8. The UFMylation pathway is impaired in Alzheimer's disease.bioRxiv : the preprint server for biology · 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

13 authors at 3 institutions in 2 countries.

Aderbal R T SilvaLaboratory of Clinical Pathology - Laboratory of Medical Investigations 23 (LIM 23), Department and Institute of Psychiatry, University of São Paulo, Medical School, São Paulo, Brazil.
Ana Cecília Feio SantosLaboratory of Clinical Pathology - Laboratory of Medical Investigations 23 (LIM 23), Department and Institute of Psychiatry, University of São Paulo, Medical School, São Paulo, Brazil.
Jose M FarfelBrazilian Brain Bank of the Aging Brain Study Group - Laboratory of Medical Investigations 22 (LIM 22), University of São Paulo, Medical School, São Paulo, Brazil; Division of Geriatrics, University of São Paulo, Medical School, São Paulo, Brazil.
Lea T GrinbergBrazilian Brain Bank of the Aging Brain Study Group - Laboratory of Medical Investigations 22 (LIM 22), University of São Paulo, Medical School, São Paulo, Brazil; Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, United States of America.
Renata E L FerrettiBrazilian Brain Bank of the Aging Brain Study Group - Laboratory of Medical Investigations 22 (LIM 22), University of São Paulo, Medical School, São Paulo, Brazil; Division of Geriatrics, University of São Paulo, Medical School, São Paulo, Brazil.
Antonio Hugo Jose Froes Marques CamposDepartment of Pathology, A. C. Camargo Cancer Center, São Paulo, Brazil.
Isabela Werneck CunhaDepartment of Pathology, A. C. Camargo Cancer Center, São Paulo, Brazil.
Maria Dirlei BegnamiDepartment of Pathology, A. C. Camargo Cancer Center, São Paulo, Brazil.
Rafael M RochaResearch Center (CIPE), A. C. Camargo Cancer Center, São Paulo, Brazil.
Dirce M CarraroResearch Center (CIPE), A. C. Camargo Cancer Center, São Paulo, Brazil.
Carlos Alberto de Bragança PereiraMathematics and Statistics Institute, University of São Paulo, São Paulo, Brazil.
Wilson Jacob-FilhoBrazilian Brain Bank of the Aging Brain Study Group - Laboratory of Medical Investigations 22 (LIM 22), University of São Paulo, Medical School, São Paulo, Brazil; Division of Geriatrics, University of São Paulo, Medical School, São Paulo, Brazil.
Helena BrentaniLaboratory of Clinical Pathology - Laboratory of Medical Investigations 23 (LIM 23), Department and Institute of Psychiatry, University of São Paulo, Medical School, São Paulo, Brazil.
Universidade de São Paulo · BRAC Camargo Hospital · BRUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by progressive cognitive decline associated with a featured neuropathology (neuritic plaques and neurofibrillary tangles). Several studies have implicated oxidative damage to DNA, DNA repair, and altered cell-cycle regulation in addition to cell death in AD post-mitotic neurons. However, there is a lack of studies that systematically assess those biological processes in patients with AD neuropathology but with no evidence of cognitive impairment. We evaluated markers of oxidative DNA damage (8-OHdG, H2AX), DNA repair (p53, BRCA1, PTEN), and cell-cycle (Cdk1, Cdk4, Cdk5, Cyclin B1, Cyclin D1, p27Kip1, phospho-Rb and E2F1) through immunohistochemistry and cell death through TUNEL in autopsy hippocampal tissue samples arrayed in a tissue microarray (TMA) composed of three groups: I) "clinical-pathological AD" (CP-AD)--subjects with neuropathological AD (Braak ≥ IV and CERAD = B or C) and clinical dementia (CDR ≥ 2, IQCODE>3.8); II) "pathological AD" (P-AD)--subjects with neuropathological AD (Braak ≥ IV and CERAD = B or C) and without cognitive impairment (CDR 0, IQCODE<3.2); and III) "normal aging" (N)--subjects without neuropathological AD (Braak ≤ II and CERAD 0 or A) and with normal cognitive function (CDR 0, IQCODE<3.2). Our results show that high levels of oxidative DNA damage are present in all groups. However, significant reductions in DNA repair and cell-cycle inhibition markers and increases in cell-cycle progression and cell death markers in subjects with CP-AD were detected when compared to both P-AD and N groups, whereas there were no significant differences in the studied markers between P-AD individuals and N subjects. This study indicates that, even in the setting of pathological AD, healthy cognition may be associated with a preserved repair to DNA damage, cell-cycle regulation, and cell death in post-mitotic neurons.

Indexed as

ApoptosisDNA DamageDNA RepairAged, 80 and overAlzheimer DiseaseCell CycleFemaleHippocampusHumansMaleNeuronsOxidative StressTissue Array AnalysisTranscriptome

Identifiers

PMID24936870
PMCPMC4061071
OpenAlexW2129162505

What OpenQuestion holds

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LicenceCC BY
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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.