Evidence map›Paper›PMID 21673973›Full record

ArticlePloS one2011

Characterization of a Drosophila Alzheimer's disease model: pharmacological rescue of cognitive defects.

Ranjita Chakraborty, Vidya Vepuri, Siddhita D Mhatre, Brie E Paddock, Sean Miller, Sarah J Michelson, Radha Delvadia, Arkit Desai, Marianna Vinokur, David J Melicharek and 9 more

Abstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
–field-weighted citation impact
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

72 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Journal of biosciences · 2023
    Review
  15. Markers and mechanisms of death inFrontiers in aging · 2023
    Article
  16. Article
  17. Sleep benefits different stages of memory inFrontiers in physiology · 2023
    Review
  18. Article
  19. Review
  20. Article

12 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

19 authors.

Ranjita ChakrabortyDepartment of Biology, Drexel University, Philadelphia, Pennsylvania, United States of America.
Vidya Vepuri
Siddhita D Mhatre
Brie E Paddock
Sean Miller
Sarah J Michelson
Radha Delvadia
Arkit Desai
Marianna Vinokur
David J Melicharek
Suruchi Utreja
Preeti Khandelwal
Sara Ansaloni
Lee E Goldstein
Robert D Moir
Jeremy C Lee
Loni P Tabb
Aleister J Saunders
Daniel R Marenda

Funding

The Abeta protein of Alzheimer's Disease is an antimicrobial peptideR01AI081990 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI MOIR, ROBERT D · 2010 to 2014
$2.2M
Identification and Characterization of APP Metabolism RegulatorsR01NS057295 · NINDS · DREXEL UNIVERSITY · PI SAUNDERS, ALEISTER J. · 2008 to 2012
$1.6M
Characterization of a novel Drosophila disease model for CHARGE SyndromeR21RR026074 · NCRR · DREXEL UNIVERSITY · PI MARENDA, DANIEL R · 2010 to 2011
$421k
NCRR NIH HHS R21 RR026074NCRR NIH HHS R21RR026074NIAID NIH HHS 1R01AI081990-01A1NIAID NIH HHS R01 AI081990NINDS NIH HHS R01 NS057295NINDS NIH HHS R01NS057295
6 · The paper itself

Abstract

Transgenic models of Alzheimer's disease (AD) have made significant contributions to our understanding of AD pathogenesis, and are useful tools in the development of potential therapeutics. The fruit fly, Drosophila melanogaster, provides a genetically tractable, powerful system to study the biochemical, genetic, environmental, and behavioral aspects of complex human diseases, including AD. In an effort to model AD, we over-expressed human APP and BACE genes in the Drosophila central nervous system. Biochemical, neuroanatomical, and behavioral analyses indicate that these flies exhibit aspects of clinical AD neuropathology and symptomology. These include the generation of Aβ(40) and Aβ(42), the presence of amyloid aggregates, dramatic neuroanatomical changes, defects in motor reflex behavior, and defects in memory. In addition, these flies exhibit external morphological abnormalities. Treatment with a γ-secretase inhibitor suppressed these phenotypes. Further, all of these phenotypes are present within the first few days of adult fly life. Taken together these data demonstrate that this transgenic AD model can serve as a powerful tool for the identification of AD therapeutic interventions.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsBehavior, AnimalBrainCarbamatesCognitionDipeptidesDisease Models, AnimalDrosophila melanogasterDrug Evaluation, PreclinicalFemaleGene Expression Regulation, EnzymologicHumansMaleAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesCarbamatesDipeptidesL 685458Protease Inhibitors

Identifiers

PMID21673973
PMCPMC3108982

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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.