Evidence map›Paper›PMID 32804126›Full record

ArticleJournal of Alzheimer's disease : JAD2020

Mitochondrial DNA Manipulations Affect Tau Oligomerization.

Ian W Weidling, Heather M Wilkins, Scott J Koppel, Lewis Hutfles, Xiaowan Wang, Anuradha Kalani, Blaise W Menta, Benjamin Ryan, Judit Perez-Ortiz, T Chris Gamblin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A blood based mitochondrial functional index biomarker for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Mitochondrial DNA affects tau phosphorylation in aging and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  11. Review
  12. Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Editorial: Systemic implications of Alzheimer's disease.Frontiers in aging neuroscience · 2023
    Article
  18. Article
  19. Article
  20. The Role of Bioenergetics in Neurodegeneration.International journal of molecular sciences · 2022
    Review
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 2 institutions in 1 country.

Ian W WeidlingUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Heather M WilkinsUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Scott J KoppelUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Lewis HutflesUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Xiaowan WangUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Anuradha KalaniUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Blaise W MentaUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Benjamin RyanUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
Judit Perez-OrtizUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
T Chris GamblinDepartment of Molecular Biosciences, University of Kansas, Lawrence, KS, USA.
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Center; the University of Kansas Medical Center, Kansas City, KS, USA.
University of Kansas Medical Center · USUniversity of Kansas · US

Funding

Transgenic & Gene-Targeting Shared ResourceP30CA168524 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOLE L NOLLEN · 2012 to 2026
$40.1M
University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JEFFREY Murray BURNS, RUSSELL H. SWERDLOW · 2021 to 2026
$25.3M
University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Kansas University Training Program in Neurological and Rehabilitation SciencesT32HD057850 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jacob J. Sosnoff · 2009 to 2026
$3.4M
NCI NIH HHS P30 CA168524NIA NIH HHS P30 AG035982NIA NIH HHS P30 AG072973NICHD NIH HHS T32 HD057850NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

backgroundMitochondrial dysfunction and tau aggregation occur in Alzheimer's disease (AD), and exposing cells or rodents to mitochondrial toxins alters their tau.

objectiveTo further explore how mitochondria influence tau, we measured tau oligomer levels in human neuronal SH-SY5Y cells with different mitochondrial DNA (mtDNA) manipulations.

methodsSpecifically, we analyzed cells undergoing ethidium bromide-induced acute mtDNA depletion, ρ0 cells with chronic mtDNA depletion, and cytoplasmic hybrid (cybrid) cell lines containing mtDNA from AD subjects.

resultsWe found cytochrome oxidase activity was particularly sensitive to acute mtDNA depletion, evidence of metabolic re-programming in the ρ0 cells, and a relatively reduced mtDNA content in cybrids generated through AD subject mitochondrial transfer. In each case tau oligomer levels increased, and acutely depleted and AD cybrid cells also showed a monomer to oligomer shift.

conclusionWe conclude a cell's mtDNA affects tau oligomerization. Overlapping tau changes across three mtDNA-manipulated models establishes the reproducibility of the phenomenon, and its presence in AD cybrids supports its AD-relevance.

Indexed as

Cell CycleCell Line, TumorCohort StudiesDNA, MitochondrialEthidiumHumansMitochondriatau ProteinsDNA, MitochondrialEthidiumMAPT protein, humantau ProteinsAlzheimer’s diseasemitochondriamitochondrial DNAoligomerstau

Identifiers

PMID32804126
PMCPMC7962146
OpenAlexW3048537844

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.