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A systems biology approach to Down syndrome: identification of Notch/Wnt dysregulation in a model of stem cells aging
Cairney CJ, Sanguinetti G, Ranghini E, Chantry AD, Nostro MC, Bhattacharyya A, Svendsen CN, Keith WN et al.. Biochimica et biophysica acta, 2009-02-06
Topic: Brain proteins, microglia and lab models
Plain-language summary
Stem cells are central to the development and maintenance of many tissues. This is due to their capacity for extensive proliferation and differentiation into effector cells. More recently it has been shown that the proliferative and differentiative ability of stem cells decreases with age, suggesting that this may play a role in tissue aging. Down syndrome (DS), is associated with many of the signs of premature tissue aging including T-cell deficiency, increased incidence of early Alzheimer-type, Myelodysplastic-type disease and leukaemia. Previously we have shown that both hematopoietic (HSC) and neural stem cells (NSC) in patients affected by DS showed signs of accelerated aging. In this study we tested the hypothesis that changes in gene expression in HSC and NSC of patients affected by DS reflect changes occurring in stem cells with age. The profiles of genes expressed in HSC and NSC from DS patients highlight pathways associated with cellular aging including a downregulation of DNA repair genes and increases in proapoptotic genes, s-phase cell cycle genes, inflammation and angiogenesis genes. Interestingly, Notch signaling was identified as a potential hub, which when deregulated may drive stem cell aging. These data suggests that DS is a valuable model to study early events in stem cell aging.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Cairney, C. J., Sanguinetti, G., Ranghini, E., Chantry, A. D., Nostro, M. C., Bhattacharyya, A., et al. (2009). A systems biology approach to Down syndrome: identification of Notch/Wnt dysregulation in a model of stem cells aging. Biochimica et biophysica acta. https://doi.org/10.1016/j.bbadis.2009.01.015
Vancouver
Cairney CJ, Sanguinetti G, Ranghini E, Chantry AD, Nostro MC, Bhattacharyya A, et al. A systems biology approach to Down syndrome: identification of Notch/Wnt dysregulation in a model of stem cells aging. Biochimica et biophysica acta. 2009. doi:10.1016/j.bbadis.2009.01.015. PMID: 19419698.
BibTeX
@article{cairney2009-19419698,
author = {Cairney, C. J. and Sanguinetti, G. and Ranghini, E. and Chantry, A. D. and Nostro, M. C. and Bhattacharyya, A. and Svendsen, C. N. and Keith, W. N. and others},
title = {{A systems biology approach to Down syndrome: identification of Notch/Wnt dysregulation in a model of stem cells aging}},
journal = {Biochimica et biophysica acta},
year = {2009},
doi = {10.1016/j.bbadis.2009.01.015},
pmid = {19419698},
url = {https://doi.org/10.1016/j.bbadis.2009.01.015}
}
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
- More recently it has been shown that the proliferative and differentiative ability of stem cells decreases with age, suggesting that this may play a role in tissue aging.
- Down syndrome (DS), is associated with many of the signs of premature tissue aging including T-cell deficiency, increased incidence of early Alzheimer-type, Myelodysplastic-type disease and leukaemia.
- Previously we have shown that both hematopoietic (HSC) and neural stem cells (NSC) in patients affected by DS showed signs of accelerated aging.
- The profiles of genes expressed in HSC and NSC from DS patients highlight pathways associated with cellular aging including a downregulation of DNA repair genes and increases in proapoptotic genes, s-phase cell cycle genes, inflammation and angiogenesis genes.
- These data suggests that DS is a valuable model to study early events in stem cell aging.
Why it matters
This study looked at gene expression in stem cells from people with Down syndrome and found changes linked to aging, including Notch signaling. It is a laboratory study of cells and does not test any treatment or prevention for Alzheimer disease.
Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, so that was left out: it earned 36 of the 96 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biochimica et biophysica acta) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2009 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization 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 | 1 / 5 | 2.2 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 3 / 6 | Cited 4.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Ilaria Bellantuono: h-index 30 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Glasgow: institution h-index 1,600 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19419698) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 36 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 36 of the 96 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.bbadis.2009.01.015
- PubMed: 19419698
- Original source →
- Free full text: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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