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Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome
Hamlett ED, Boger HA, Ledreux A, Kelley CM, Mufson EJ, Falangola MF, Guilfoyle DN, Nixon RA et al.. Current Alzheimer research, 2016-01-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America. DS is characterized by complete or segmental chromosome 21 trisomy, which leads to variable intellectual disabilities, progressive memory loss, and accelerated neurodegeneration with age. During the last three decades, people with DS have experienced a doubling of life expectancy due to progress in treatment of medical comorbidities, which has allowed this population to reach the age when they develop early onset Alzheimer's disease (AD). Individuals with DS develop cognitive and pathological hallmarks of AD in their fourth or fifth decade, and are currently lacking successful prevention or treatment options for dementia. The profound memory deficits associated with DS-related AD (DS-AD) have been associated with degeneration of several neuronal populations, but mechanisms of neurodegeneration are largely unexplored. The most successful animal model for DS is the Ts65Dn mouse, but several new models have also been developed. In the current review, we discuss recent findings and potential treatment options for the management of memory loss and AD neuropathology in DS mouse models. We also review agerelated neuropathology, and recent findings from neuroimaging studies. The validation of appropriate DS mouse models that mimic neurodegeneration and memory loss in humans with DS can be valuable in the study of novel preventative and treatment interventions, and may be helpful in pinpointing gene-gene interactions as well as specific gene segments involved in neurodegeneration.
What this study adds
Evidence grade: Low
This is a narrative review. This review discusses memory loss and Alzheimer pathology in mouse models of Down syndrome and notes that mechanisms of nerve cell degeneration are largely unexplored. It reports no treatment or cure.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Hamlett, E. D., Boger, H. A., Ledreux, A., Kelley, C. M., Mufson, E. J., Falangola, M. F., et al. (2016). Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome. Current Alzheimer research. https://doi.org/10.2174/1567205012666150921095505
Vancouver
Hamlett ED, Boger HA, Ledreux A, Kelley CM, Mufson EJ, Falangola MF, et al. Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome. Current Alzheimer research. 2016. doi:10.2174/1567205012666150921095505. PMID: 26391050.
BibTeX
@article{hamlett2016-26391050,
author = {Hamlett, E. D. and Boger, H. A. and Ledreux, A. and Kelley, C. M. and Mufson, E. J. and Falangola, M. F. and Guilfoyle, D. N. and Nixon, R. A. and others},
title = {{Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome}},
journal = {Current Alzheimer research},
year = {2016},
doi = {10.2174/1567205012666150921095505},
pmid = {26391050},
url = {https://doi.org/10.2174/1567205012666150921095505}
}
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.
Key findings
- The profound memory deficits associated with DS-related AD (DS-AD) have been associated with degeneration of several neuronal populations, but mechanisms of neurodegeneration are largely unexplored.
Why it matters
This review discusses memory loss and Alzheimer pathology in mouse models of Down syndrome and notes that mechanisms of nerve cell degeneration are largely unexplored. It reports no treatment or cure.
Study details
- Evidence strengthLow
How this study scored 37/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current Alzheimer research) |
| Journal's citation record | 1 / 4 | Current Alzheimer Research: journal h-index 119 (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 | 2016 — 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 |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 50 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.2 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 3 / 6 | Cited 3.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ann‐Charlotte Granholm: h-index 58 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Medical University of South Carolina: institution h-index 715 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26391050) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.2174/1567205012666150921095505
- PubMed: 26391050
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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