Evidence map›Paper›PMID 31053140›Full record

ArticleMolecular brain2019

Brain transcriptome analysis of a familial Alzheimer's disease-like mutation in the zebrafish presenilin 1 gene implies effects on energy production.

Morgan Newman, Nhi Hin, Stephen Pederson, Michael Lardelli

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

15 citing papers in PubMed, 56 citations in OpenAlex.

  1. ZL006 Treatment Reduces Inflammation, Oxidative Stress, and Brain AβInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. In-Frame and Frameshift Mutations in ZebrafishJournal of Alzheimer's disease reports · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Iron-responsive-like elements and neurodegenerative ferroptosis.Learning & memory (Cold Spring Harbor, N.Y.) · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Article
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

4 authors at 1 institution in 1 country.

Morgan NewmanDepartment of Molecular and Biomedical Science, University of Adelaide, School of Biological Sciences, North Terrace, Adelaide, SA, 5005, Australia.
Nhi HinDepartment of Molecular and Biomedical Science, University of Adelaide, School of Biological Sciences, North Terrace, Adelaide, SA, 5005, Australia.
Stephen PedersonDepartment of Molecular and Biomedical Science, University of Adelaide, School of Biological Sciences, North Terrace, Adelaide, SA, 5005, Australia.
Michael LardelliDepartment of Molecular and Biomedical Science, University of Adelaide, School of Biological Sciences, North Terrace, Adelaide, SA, 5005, Australia. Michael.lardelli@adelaide.edu.au.ORCID 0000-0002-4289-444X
The University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To prevent or ameliorate Alzheimer's disease (AD) we must understand its molecular basis. AD develops over decades but detailed molecular analysis of AD brains is limited to postmortem tissue where the stresses initiating the disease may be obscured by compensatory responses and neurodegenerative processes. Rare, dominant mutations in a small number of genes, but particularly the gene PRESENILIN 1 (PSEN1), drive early onset of familial AD (EOfAD). Numerous transgenic models of AD have been constructed in mouse and other organisms, but transcriptomic analysis of these models has raised serious doubts regarding their representation of the disease state. Since we lack clarity regarding the molecular mechanism(s) underlying AD, we posit that the most valid approach is to model the human EOfAD genetic state as closely as possible. Therefore, we sought to analyse brains from zebrafish heterozygous for a single, EOfAD-like mutation in their PSEN1-orthologous gene, psen1. We previously introduced an EOfAD-like mutation (Q96_K97del) into the endogenous psen1 gene of zebrafish. Here, we analysed transcriptomes of young adult (6-month-old) entire brains from a family of heterozygous mutant and wild type sibling fish. Gene ontology (GO) analysis implies effects on mitochondria, particularly ATP synthesis, and on ATP-dependent processes including vacuolar acidification.

Indexed as

Gene Expression ProfilingAlzheimer DiseaseAnimalsBrainEnergy MetabolismGene Expression RegulationGene OntologyHeterozygoteHumansMutationPresenilin-1ZebrafishZebrafish ProteinsPresenilin-1Psen1 protein, zebrafishZebrafish ProteinsAlzheimer’s diseaseATP synthesisBrainGenome editingMitochondriaMutationPresenilin 1TranscriptomeVacuolar acidificationZebrafish

Identifiers

PMID31053140
PMCPMC6500017
OpenAlexW2944989878

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.