Evidence map›Paper›PMID 23740939›Full record

ArticleHuman molecular genetics2013

Bioenergetic flux, mitochondrial mass and mitochondrial morphology dynamics in AD and MCI cybrid cell lines.

Diana F Silva, J Eva Selfridge, Jianghua Lu, Lezi E, Nairita Roy, Lewis Hutfles, Jeffrey M Burns, Elias K Michaelis, ShiDu Yan, Sandra M Cardoso and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
4.5field-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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Mitochondrial DNA affects tau phosphorylation in aging and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024
    Review
  9. Article
  10. Intraneuronal β-amyloid impaired mitochondrial proteostasis through the impact on LONP1.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Role of Bioenergetics in Neurodegeneration.International journal of molecular sciences · 2022
    Review

31 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

11 authors at 4 institutions in 3 countries.

Diana F Silva
J Eva Selfridge
Jianghua Lu
Lezi E
Nairita Roy
Lewis Hutfles
Jeffrey M Burns
Elias K Michaelis
ShiDu Yan
Sandra M Cardoso
Russell H Swerdlow
University of Kansas · USCenter for Neurosciences · USLaboratoire d’immunologie intégrative du cancer · FRUniversity of Kansas Medical Center · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
NIA NIH HHS P30 AG035982NIA NIH HHS P30AG035982
6 · The paper itself

Abstract

Bioenergetic dysfunction occurs in Alzheimer's disease (AD) and mild cognitive impairment (MCI), a clinical syndrome that frequently precedes symptomatic AD. In this study, we modeled AD and MCI bioenergetic dysfunction by transferring mitochondria from MCI, AD and control subject platelets to mtDNA-depleted SH-SY5Y cells. Bioenergetic fluxes and bioenergetics-related infrastructures were characterized in the resulting cytoplasmic hybrid (cybrid) cell lines. Relative to control cybrids, AD and MCI cybrids showed changes in oxygen consumption, respiratory coupling and glucose utilization. AD and MCI cybrids had higher ADP/ATP and lower NAD+/NADH ratios. AD and MCI cybrids exhibited differences in proteins that monitor, respond to or regulate cell bioenergetic fluxes including HIF1α, PGC1α, SIRT1, AMPK, p38 MAPK and mTOR. Several endpoints suggested mitochondrial mass increased in the AD cybrid group and probably to a lesser extent in the MCI cybrid group, and that the mitochondrial fission-fusion balance shifted towards increased fission in the AD and MCI cybrids. As many of the changes we observed in AD and MCI cybrid models are also seen in AD subject brains, we conclude reduced bioenergetic function is present during very early AD, is not brain-limited and induces protean retrograde responses that likely have both adaptive and mal-adaptive consequences.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAMP-Activated Protein KinasesCarrier ProteinsCase-Control StudiesCell LineCognitive DysfunctionDNA, MitochondrialEnergy MetabolismHumansHybrid CellsHypoxia-Inducible Factor 1, alpha SubunitMiddle AgedMitochondriaMitochondrial DynamicsAMP-Activated Protein KinasesCarrier ProteinsDNA, MitochondrialHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMTOR protein, humanPPARGC1B protein, humanReactive Oxygen SpeciesRNA-Binding ProteinsSIRT1 protein, humanSirtuin 1TOR Serine-Threonine Kinases

Identifiers

PMID23740939
PMCPMC3888119
OpenAlexW2119278281

What OpenQuestion holds

Textmetadata
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.