Evidence map›Paper›PMID 20302939›Full record

ReviewNeurobiology of disease2010

Alzheimer's disease and tauopathy studies in flies and worms.

Jill Wentzell, Doris Kretzschmar

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  3. Review
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  8. Review
  9. Restoration of Olfactory Memory inFrontiers in cellular neuroscience · 2019
    Article
  10. Alzheimer's Disease and Sleep-Wake Disturbances: Amyloid, Astrocytes, and Animal Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Review
  11. What Can We Learn About Human Disease from the Nematode C. elegans?Methods in molecular biology (Clifton, N.J.) · 2018
    Review
  12. Glial Draper Rescues Aβ Toxicity in aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Review
  14. Mass Histology to Quantify Neurodegeneration in Drosophila.Journal of visualized experiments : JoVE · 2016
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Jill WentzellCenter for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, OR 97239, USA.
Doris Kretzschmar
Oregon Health & Science University · US

Funding

SWS/NTE function in neurodegeneration and axonopathyR01NS047663 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI KRETZSCHMAR, DORIS · 2004 to 2013
$2.7M
NINDS NIH HHS R01 NS047663
6 · The paper itself

Abstract

Progressive dementias like Alzheimer's Disease (AD) and other tauopathies are an increasing threat to human health worldwide. Although significant progress has been made in understanding the pathogenesis of these diseases using cell culture and mouse models, the complexity of these diseases has still prevented a comprehensive understanding of their underlying causes. As with other neurological diseases, invertebrate models have provided novel genetic approaches for investigating the molecular pathways that are affected in tauopathies, including AD. This review focuses on transgenic models that have been established in Drosophila melanogaster and Caenorhabditis elegans to investigate these diseases, and the insights that have been gained from these studies. Also included are a brief description of the endogenous versions of human "disease genes" (like tau and the Amyloid Precursor Protein) that are expressed in invertebrates, and an overview of results that have been obtained from animals lacking or overexpressing these genes. These diverse models can be used to advance our knowledge about how these proteins acquire a pathogenic function and how disrupting their normal functions may contribute to neurological pathologies. They also provide powerful assays for identifying molecular and genetic interactions that are important in developing or preventing the deleterious effects.

Indexed as

Models, GeneticAlzheimer DiseaseAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansDrosophila melanogasterGene Expression RegulationGenetic Predisposition to DiseaseHumansMolecular BiologyTauopathiesTransgenes

Identifiers

PMID20302939
PMCPMC2894260
OpenAlexW1971515849

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.