Evidence map›Paper›PMID 26729583›Full record

ArticleScientific reports2016

Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease.

Liang Zhang, Sergey Trushin, Trace A Christensen, Benjamin V Bachmeier, Benjamin Gateno, Andreas Schroeder, Jia Yao, Kie Itoh, Hiromi Sesaki, Wayne W Poon and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

135 citing papers in PubMed, 203 citations in OpenAlex.

  1. Article
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  9. Mitochondrial pearling: membrane biophysics, CaFrontiers in cell and developmental biology · 2026
    Review
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75 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

16 authors at 7 institutions in 1 country.

Liang ZhangDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Sergey TrushinDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Trace A ChristensenElectron Microscopy Core Facility, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Benjamin V BachmeierDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Benjamin GatenoDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Andreas SchroederDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Jia YaoDepartment of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, USA.
Kie ItohDepartment of Cell Biology, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD, USA.
Hiromi SesakiDepartment of Cell Biology, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD, USA.
Wayne W PoonInstitute for Memory Impairments and Neurological Disorders. University of California Irvine, CA, USA.
Karen H GylysUCLA School of Nursing, CA, USA.
Emily R PattersonLaboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
Joseph E ParisiLaboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
Roberta Diaz BrintonDepartment of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, USA.
Jeffrey L SalisburyElectron Microscopy Core Facility, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Eugenia TrushinaDepartment of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Mayo Clinic · USMayo Clinic in Arizona · USUniversity of Southern California · USJohns Hopkins Medicine · USJohns Hopkins University · USUCLA Health · USUniversity of California, Irvine · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 1985 to 2018
$24.8M
Mitochondrial Complex I as a Target for Neuroprotection in ADRF1AG055549 · NIA · MAYO CLINIC ROCHESTER · PI TRUSHINA, EUGENIA · 2017 to 2025
$7.0M
Mitochondrial Fusion and DivisionR01GM089853 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI SESAKI, HIROMI · 2010 to 2014
$2.1M
Mitochondrial dynamics and metabolomic biomarkers in neurodegenerative disordersR01ES020715 · NIEHS · MAYO CLINIC ROCHESTER · PI TRUSHINA, EUGENIA · 2011 to 2015
$1.8M
ApoE and cholesterol effects on amyloid beta in synaptic terminals in ADR56AG027465 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GYLYS, KAREN H · 2015 to 2015
$385k
NCATS NIH HHS UL1 TR000135NIA NIH HHS P01 AG000538NIA NIH HHS P50 AG016573NIA NIH HHS R56 AG027465NIA NIH HHS RF1 AG055549NIEHS NIH HHS R01 ES020715NIEHS NIH HHS R01ES020715NIGMS NIH HHS GM089853NIGMS NIH HHS R01 GM089853
6 · The paper itself

Abstract

Altered brain metabolism is associated with progression of Alzheimer's Disease (AD). Mitochondria respond to bioenergetic changes by continuous fission and fusion. To account for three dimensional architecture of the brain tissue and organelles, we applied 3-dimensional electron microscopy (3D EM) reconstruction to visualize mitochondrial structure in the brain tissue from patients and mouse models of AD. We identified a previously unknown mitochondrial fission arrest phenotype that results in elongated interconnected organelles, "mitochondria-on-a-string" (MOAS). Our data suggest that MOAS formation may occur at the final stages of fission process and was not associated with altered translocation of activated dynamin related protein 1 (Drp1) to mitochondria but with reduced GTPase activity. Since MOAS formation was also observed in the brain tissue of wild-type mice in response to hypoxia or during chronological aging, fission arrest may represent fundamental compensatory adaptation to bioenergetic stress providing protection against mitophagy that may preserve residual mitochondrial function. The discovery of novel mitochondrial phenotype that occurs in the brain tissue in response to energetic stress accurately detected only using 3D EM reconstruction argues for a major role of mitochondrial dynamics in regulating neuronal survival.

Indexed as

Energy MetabolismMitochondrial DynamicsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrainCA1 Region, HippocampalDisease Models, AnimalDynaminsHypoxiaMice, KnockoutMice, TransgenicMitochondriaPhenotypePhosphorylationAmyloid beta-Protein PrecursorDnm1l protein, mouseDynamins

Identifiers

PMID26729583
PMCPMC4700525
OpenAlexW2224041865

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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.