Evidence map›Paper›PMID 30612335›Full record

ArticleMolecular neurobiology2019

Amyloid Precursor Protein Mediates Neuronal Protection from Rotenone Toxicity.

Kathryn Cimdins, Hayley S Waugh, Vicki Chrysostomou, M Isabel G Lopez Sanchez, Vanessa A Johannsen, Mark J Cook, Jonathan G Crowston, Andrew F Hill, James A Duce, Ashley I Bush and 1 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Ethyl maltol disrupt iron homeostasis in SH-SY5Y neuroblastoma cell line.Journal of biochemical and molecular toxicology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Kathryn CimdinsCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia.
Hayley S WaughCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia.
Vicki ChrysostomouCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia.
M Isabel G Lopez SanchezCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia.
Vanessa A JohannsenDepartment of Oncology, University of Oxford, Oxford, UK.
Mark J CookDepartment of Medicine, St. Vincent's Hospital, The University of Melbourne, 75 Commercial Road, Melbourne, Victoria, 3004, Australia.
Jonathan G CrowstonCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia.
Andrew F HillDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Victoria, Australia.
James A DuceThe ALBORADA Drug Discovery Institute, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Ashley I BushThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia.
Ian A TrounceCentre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia. i.trounce@unimelb.edu.au.ORCID http://orcid.org/0000-0002-1070-8892
The University of Melbourne · AULa Trobe University · AUUniversity of Oxford · GB

Funding

BrightFocus Foundation G2009020
6 · The paper itself

Abstract

Mitochondrial complex I dysfunction is the most common respiratory chain defect in human disorders and a hotspot for neurodegenerative diseases. Amyloid precursor protein (APP) and its non-amyloidogenic processing products, in particular soluble APP α (sAPPα), have been shown to provide neuroprotection in models of neuronal injury; however, APP-mediated protection from acute mitochondrial injury has not been previously reported. Here, we use the plant-derived pesticide rotenone, a potent complex I-specific mitochondrial inhibitor, to discover neuroprotective effects of APP and sAPPα in vitro, in neuronal cell lines over-expressing APP, and in vivo, in a retinal neuronal rotenone toxicity mouse model. Our results show that APP over-expression is protective against rotenone toxicity in neurons via sAPPα through an autocrine/paracrine mechanism that involves the Pi3K/Akt pro-survival pathway. APP

Indexed as

Toxicity TestsAdenosine TriphosphateAdolescentAdultAgedAged, 80 and overAgingAmyloid beta-Protein PrecursorAnimalsCell Line, TumorChildChild, PreschoolEnzyme ActivationFemaleHumansMaleAdenosine TriphosphateAmyloid beta-Protein PrecursorNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesRotenoneAmyloid precursor proteinComplex IMitochondriaNeuroprotectionRetinaRotenone

Identifiers

PMID30612335
PMCPMC6614131
OpenAlexW2906879568

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.