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Dissecting Alzheimer disease in Down syndrome using mouse models
Choong XY, Tosh JL, Pulford LJ, Fisher EM.. Frontiers in behavioral neuroscience, 2015-10-13
Topic: Amyloid, tau and blood-test diagnosis
Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21). This greatly increases the risk of Alzheimer disease (AD), but although virtually all people with DS have AD neuropathology by 40 years of age, not all develop dementia. To dissect the genetic contribution of trisomy 21 to DS phenotypes including those relevant to AD, a range of DS mouse models has been generated which are trisomic for chromosome segments syntenic to human chromosome 21. Here, we consider key characteristics of human AD in DS (AD-DS), and our current state of knowledge on related phenotypes in AD and DS mouse models. We go on to review important features needed in future models of AD-DS, to understand this type of dementia and so highlight pathogenic mechanisms relevant to all populations at risk of AD.
Key findings
- Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21).
- This greatly increases the risk of Alzheimer disease (AD), but although virtually all people with DS have AD neuropathology by 40 years of age, not all develop dementia.
- To dissect the genetic contribution of trisomy 21 to DS phenotypes including those relevant to AD, a range of DS mouse models has been generated which are trisomic for chromosome segments syntenic to human chromosome 21.
- Here, we consider key characteristics of human AD in DS (AD-DS), and our current state of knowledge on related phenotypes in AD and DS mouse models.
- We go on to review important features needed in future models of AD-DS, to understand this type of dementia and so highlight pathogenic mechanisms relevant to all populations at risk of AD.
Why it matters
This review describes mouse models used to study Alzheimer disease in Down syndrome and notes that not all people with Down syndrome who have Alzheimer neuropathology develop dementia. It discusses what future models need, but it does not report a treatment or prevention for Alzheimer disease.
Study details
- Evidence strengthLow
How this study scored 40/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in behavioral neuroscience) |
| Journal's citation record | 1 / 4 | Frontiers in Behavioral Neuroscience: journal h-index 138 (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 | 2015 — within 20 year(s) of the newest study here |
| 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 | 4 / 7 | Cited 42 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.2 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 3 / 6 | Cited 5.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 0 / 4 | Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Elizabeth Fisher: h-index 84 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26528151) |
| Free to read | 2 / 2 | Free to read |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnbeh.2015.00268
- PubMed: 26528151
- Original source →
- Free full text: Frontiers in Behavioral Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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. Check the citation against the original before you use it.
APA 7th
Choong, X. Y., Tosh, J. L., Pulford, L. J., & Fisher, E. M. (2015). Dissecting Alzheimer disease in Down syndrome using mouse models. Frontiers in behavioral neuroscience. https://doi.org/10.3389/fnbeh.2015.00268
Vancouver
Choong XY, Tosh JL, Pulford LJ, Fisher EM. Dissecting Alzheimer disease in Down syndrome using mouse models. Frontiers in behavioral neuroscience. 2015. doi:10.3389/fnbeh.2015.00268. PMID: 26528151.
BibTeX
@article{choong2015-26528151,
author = {Choong, X. Y. and Tosh, J. L. and Pulford, L. J. and Fisher, E. M.},
title = {{Dissecting Alzheimer disease in Down syndrome using mouse models}},
journal = {Frontiers in behavioral neuroscience},
year = {2015},
doi = {10.3389/fnbeh.2015.00268},
pmid = {26528151},
url = {https://doi.org/10.3389/fnbeh.2015.00268}
}
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