Evidence map›Paper›PMID 19720087›Full record

ArticleBehavioural brain research2010

Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6b(rd1).

Alberto C S Costa, Melissa R Stasko, Cecilia Schmidt, Muriel T Davisson

Abstract readValidation Study
In one paragraph

Article in Behavioural brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Article
  2. Role of cystathionine-β-synthase and hydrogen sulfide in down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  3. Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mouse models of aneuploidy to understand chromosome disorders.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Review
  14. Article
  15. Behavioral Phenotyping for Down Syndrome in Mice.Current protocols in mouse biology · 2020
    Article
  16. Article
  17. Article
  18. Influence of allelic differences in Down syndrome.Progress in brain research · 2020
    Review
  19. Exosome release and cargo in Down syndrome.Developmental neurobiology · 2019
    Review
  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

4 authors.

Alberto C S CostaDivision of Clinical Pharmacology and Toxicology, Department of Medicine, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA. Alberto.Costa@ucdenver.edu
Melissa R Stasko
Cecilia Schmidt
Muriel T Davisson

Funding

Systems Biology for Studies of Cognition in Down SyndromeR01HD056235 · NICHD · UNIVERSITY OF COLORADO DENVER · PI GARDINER, KATHELEEN · 2008 to 2012
$2.7M
A REPOSITORY OF MOUSE MODELS FOR CYTOGENETIC DISORDERSN01HD073265 · NICHD · JACKSON LABORATORY · PI DAVISSON, MURIEL T · 1997 to 2000
$355k
NICHD NIH HHS HD056235NICHD NIH HHS HD73265NICHD NIH HHS R01 HD056235
6 · The paper itself

Abstract

The Ts65Dn mouse is the most studied and complete aneuploid model of Down syndrome (DS) widely available. As a model for human trisomy 21, these mice display many attractive features, including performance deficits in different behavioral tasks, alterations in synaptic plasticity and adult neurogenesis, motor dysfunction, and age-dependent cholinergic neurodegeneration. Currently, Ts65Dn mice are maintained on a genetic background that leads to blindness in about 25% of their offspring, because it segregates for the retinal degeneration 1 (Pde6b(rd1)) mutation of C3H/HeSnJ. This means that 25% of the mice have to be discarded in most experiments involving these animals, which is particularly problematic because the Ts65Dn stock has low reproductive performance. To circumvent this problem, we have bred the Ts65Dn extra chromosome many generations into a closely related genetic background that does not carry the Pde6b(rd1) mutation. Although the new genetic background is expected to be nearly identical to the original, differences in genetic background have the potential to alter mouse performance in certain behavioral tests. Therefore, we designed the present study primarily as a behavioral validation of Ts65Dn mice of the new background. We compared side-by-side their performance with that of Ts65Dn mice of the original background on the following set of assessments: (1) body length and weight; (2) 24-h locomotor activity; (3) the Morris water maze; (4) fear conditioning; and (5) grip strength. Except for very subtle differences on water maze performance, we found no significant differences between Ts65Dn mice on the two backgrounds in the measures assessed.

Indexed as

PhenotypeAnalysis of VarianceAnimalsBehavior, AnimalBody SizeBody WeightConditioning, ClassicalDisease Models, AnimalDown SyndromeExploratory BehaviorFearHand StrengthMaze LearningMiceMice, Inbred C57BLMice, Transgenic

Identifiers

PMID19720087
PMCPMC2783207

What OpenQuestion holds

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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.