Evidence map›Paper›PMID 27793643›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2017

Nuclear but not mitochondrial-encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer's disease.

Diego Mastroeni, Omar M Khdour, Elaine Delvaux, Jennifer Nolz, Gary Olsen, Nicole Berchtold, Carl Cotman, Sidney M Hecht, Paul D Coleman

Open access · greenAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
4.4field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Sex-stratified genome-wide meta-analysis identifies novel loci for cognitive decline in older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  17. Neuronal ABCA7 deficiency aggravates mitochondrial dysfunction and neurodegeneration in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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9 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Diego MastroeniASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA; Banner Sun Health Research Institute, Sun City, AZ, USA. Electronic address: diego.mastroeni@asu.edu.
Omar M KhdourBiodesign Institute, and Department of Chemistry and Biochemistry, Arizona State University, Tempe, AZ, USA.
Elaine DelvauxASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA.
Jennifer NolzASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA.
Gary OlsenBanner Sun Health Research Institute, Sun City, AZ, USA.
Nicole BerchtoldInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, USA.
Carl CotmanInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, USA.
Sidney M HechtBiodesign Institute, and Department of Chemistry and Biochemistry, Arizona State University, Tempe, AZ, USA.
Paul D ColemanASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA; Banner Sun Health Research Institute, Sun City, AZ, USA.
Arizona State University · USBanner Sun Health Research Institute · USUniversity of California, Irvine · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
DNA methylation in Alzheimer?s disease and normally aged brainR01AG036400 · NIA · BANNER SUN HEALTH RESEARCH INSTITUTE · PI COLEMAN, PAUL D · 2009 to 2013
$2.0M
NCATS NIH HHS UL1 TR001414NIA NIH HHS R01 AG036400
6 · The paper itself

Abstract

introductionWe have comprehensively described the expression profiles of mitochondrial DNA and nuclear DNA genes that encode subunits of the respiratory oxidative phosphorylation (OXPHOS) complexes (I-V) in the hippocampus from young controls, age matched, mild cognitively impaired (MCI), and Alzheimer's disease (AD) subjects.

methodsHippocampal tissues from 44 non-AD controls (NC), 10 amnestic MCI, and 18 AD cases were analyzed on Affymetrix Hg-U133 plus 2.0 arrays.

resultsThe microarray data revealed significant down regulation in OXPHOS genes in AD, particularly those encoded in the nucleus. In contrast, there was up regulation of the same gene(s) in MCI subjects compared to AD and ND cases. No significant differences were observed in mtDNA genes identified in the array between AD, ND, and MCI subjects except one mt-ND6. DISCUSSION: Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression.

Indexed as

Oxidative PhosphorylationAdultAged, 80 and overAgingAlzheimer DiseaseAutopsyCognition DisordersFemaleHippocampusHumansMaleMitochondriaOligonucleotide Array Sequence AnalysisAgingAlzheimer's diseaseMicroarrayMild cognitively impaired (MCI)MitochondriaOxidative phosphorylation-related genes expressionPostmortem brains

Identifiers

PMID27793643
PMCPMC5967608
OpenAlexW2534146519

What OpenQuestion holds

Textmetadata
LicenceTDM
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.