Evidence map›Paper›PMID 25457027›Full record

ArticleNeurobiology of aging2015

Identifying Aβ-specific pathogenic mechanisms using a nematode model of Alzheimer's disease.

Wail M Hassan, Vishantie Dostal, Brady N Huemann, John E Yerg, Christopher D Link

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The Role of the Oral Microbiome in the Development of Diseases.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Vitamin BCell reports · 2021
    Article
  8. Article
  9. Article
  10. α-Sheet secondary structure in amyloid β-peptide drives aggregation and toxicity in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. What Can We Learn About Human Disease from the Nematode C. elegans?Methods in molecular biology (Clifton, N.J.) · 2018
    Review
  16. Activation of liver X receptor α protects amyloid βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  17. Review
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Wail M HassanDepartment of Biomedical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI, USA; Department of Integrative Physiology, Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO, USA. Electronic address: hassanw@uwm.edu.
Vishantie DostalDepartment of Integrative Physiology, Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO, USA.
Brady N HuemannDepartment of Biomedical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
John E YergDepartment of Integrative Physiology, Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO, USA.
Christopher D LinkDepartment of Integrative Physiology, Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO, USA.
University of Colorado Boulder · USUniversity of Wisconsin–Milwaukee · US

Funding

TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODELR01AG012423 · NIA · UNIVERSITY OF COLORADO AT BOULDER · PI LINK, CHRISTOPHER D. · 1996 to 2012
$3.6M
Comparative Modeling of Neurodegenerative DiseasesR01AG021037 · NIA · UNIVERSITY OF COLORADO AT BOULDER · PI LINK, CHRISTOPHER D. · 2003 to 2006
$1.1M
NIA NIH HHS R01 AG012423NIA NIH HHS R01 AG021037
6 · The paper itself

Abstract

Multiple gene expression alterations have been linked to Alzheimer's disease (AD), implicating multiple metabolic pathways in its pathogenesis. However, a clear distinction between AD-specific gene expression changes and those resulting from nonspecific responses to toxic aggregating proteins has not been made. We investigated alterations in gene expression induced by human beta-amyloid peptide (Aβ) in a Caenorhabditis elegans AD model. Aβ-induced gene expression alterations were compared with those caused by a synthetic aggregating protein to identify Aβ-specific effects. Both Aβ-specific and nonspecific alterations were observed. Among Aβ-specific genes were those involved in aging, proteasome function, and mitochondrial function. An intriguing observation was the significant overlap between gene expression changes induced by Aβ and those induced by Cry5B, a bacterial pore-forming toxin. This led us to hypothesize that Aβ exerts its toxic effect, at least in part, by causing damage to biological membranes. We provide in vivo evidence consistent with this hypothesis. This study distinguishes between Aβ-specific and nonspecific mechanisms and provides potential targets for therapeutics discovery.

Indexed as

Caenorhabditis elegansAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBacillus thuringiensis ToxinsBacterial ProteinsDisease Models, AnimalEndotoxinsGene ExpressionHemolysin ProteinsHumansMitochondriaMolecular Targeted TherapyProteasome Endopeptidase ComplexAmyloid beta-PeptidesBacillus thuringiensis ToxinsBacterial ProteinsEndotoxinsHemolysin Proteinsinsecticidal crystal protein, Bacillus ThuringiensisProteasome Endopeptidase ComplexAlzheimer's diseaseBeta-amyloidDementiaNeurodegenerationNeurodegenerative disorders

Identifiers

PMID25457027
PMCPMC4315719
OpenAlexW2055224091

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.