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A mouse model for Down syndrome exhibits learning and behaviour deficits
Reeves RH, Irving NG, Moran TH, Wohn A, Kitt C, Sisodia SS, Schmidt C, Bronson RT et al.. Nature genetics, 1995-10-01
Topic: Brain proteins, microglia and lab models
Trisomy 21 or Down syndrome (DS) is the most frequent genetic cause of mental retardation, affecting one in 800 live born human beings. Mice with segmental trisomy 16 (Ts65Dn mice) are at dosage imbalance for genes corresponding to those on human chromosome 21q21-22.3--which includes the so-called DS 'critical region'. They do not show early-onset of Alzheimer disease pathology; however, Ts65Dn mice do demonstrate impaired performance in a complex learning task requiring the integration of visual and spatial information. The reproducibility of this phenotype among Ts65Dn mice indicates that dosage imbalance for a gene or genes in this region contributes to this impairment. The corresponding dosage imbalance for the human homologues of these genes may contribute to cognitive deficits in DS.
Key findings
- The reproducibility of this phenotype among Ts65Dn mice indicates that dosage imbalance for a gene or genes in this region contributes to this impairment.
Why it matters
In mice carrying extra copies of genes that correspond to part of human chromosome 21 (21q21-22.3, including the Down syndrome "critical region"), the Ts65Dn model, animals performed worse on "a complex learning task requiring the integration of visual and spatial information". The authors say the reproducibility of this deficit indicates that extra dosage of "a gene or genes in this region" contributes, and that the human versions "may contribute to cognitive deficits in DS". These mice "do not show early-onset of Alzheimer disease pathology", so this is a Down syndrome learning model, not an Alzheimer's model, and it reports no treatment.
Study details
- Evidence strengthLow
How this study scored 54/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature genetics) |
| Journal's citation record | 4 / 4 | Nature Genetics: journal h-index 776 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 1995 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 914 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 27.7 citations a year over 33 year(s) since 1995 |
| Impact for its field and year | 5 / 6 | Cited 28.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 17 other studies in this library |
| Still being cited | 3 / 4 | Cited 67 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Muriel Trask Davisson: h-index 62 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Johns Hopkins University: institution h-index 2,306 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 7550346) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 54 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), so the publisher may charge for it. The PubMed abstract is free.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Reeves, R. H., Irving, N. G., Moran, T. H., Wohn, A., Kitt, C., Sisodia, S. S., et al. (1995). A mouse model for Down syndrome exhibits learning and behaviour deficits. Nature genetics. https://doi.org/10.1038/ng1095-177
Vancouver
Reeves RH, Irving NG, Moran TH, Wohn A, Kitt C, Sisodia SS, et al. A mouse model for Down syndrome exhibits learning and behaviour deficits. Nature genetics. 1995. doi:10.1038/ng1095-177. PMID: 7550346.
BibTeX
@article{reeves1995-7550346,
author = {Reeves, R. H. and Irving, N. G. and Moran, T. H. and Wohn, A. and Kitt, C. and Sisodia, S. S. and Schmidt, C. and Bronson, R. T. and others},
title = {{A mouse model for Down syndrome exhibits learning and behaviour deficits}},
journal = {Nature genetics},
year = {1995},
doi = {10.1038/ng1095-177},
pmid = {7550346},
url = {https://doi.org/10.1038/ng1095-177}
}
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