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Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis
Griffin WS, Sheng JG, McKenzie JE, Royston MC, Gentleman SM, Brumback RA, Cork LC, Del Bigio MR et al.. Neurobiology of aging, 1998-09-01
Topic: Brain proteins, microglia and lab models
Chronic overexpression of the neurite growth-promoting factor S100beta has been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease. Such plaques are virtually universal in middle-aged Down's syndrome, making Down's a natural model of Alzheimer's disease. We determined numbers of astrocytes overexpressing S100beta, and of neurons overexpressing beta-amyloid precursor protein (beta-APP), and assayed for neurofibrillary tangles in neocortex of 20 Down's syndrome patients (17 weeks gestation to 68 years).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Griffin, W. S., Sheng, J. G., McKenzie, J. E., Royston, M. C., Gentleman, S. M., Brumback, R. A., et al. (1998). Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis. Neurobiology of aging. https://doi.org/10.1016/s0197-4580(98)00074-8
Vancouver
Griffin WS, Sheng JG, McKenzie JE, Royston MC, Gentleman SM, Brumback RA, et al. Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis. Neurobiology of aging. 1998. doi:10.1016/s0197-4580(98)00074-8. PMID: 9880042.
BibTeX
@article{griffin1998-9880042,
author = {Griffin, W. S. and Sheng, J. G. and McKenzie, J. E. and Royston, M. C. and Gentleman, S. M. and Brumback, R. A. and Cork, L. C. and Del Bigio, M. R. and others},
title = {{Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis}},
journal = {Neurobiology of aging},
year = {1998},
doi = {10.1016/s0197-4580(98)00074-8},
pmid = {9880042},
url = {https://doi.org/10.1016/s0197-4580(98)00074-8}
}
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
- Such plaques are virtually universal in middle-aged Down's syndrome, making Down's a natural model of Alzheimer's disease.
- We determined numbers of astrocytes overexpressing S100beta, and of neurons overexpressing beta-amyloid precursor protein (beta-APP), and assayed for neurofibrillary tangles in neocortex of 20 Down's syndrome patients (17 weeks gestation to 68 years).
- Compared to controls, there were twice as many S100beta-immunoreactive (S100beta+) astrocytes in Down's patients at all ages: fetal, young, and adult (p = 0.01, or better, in each age group).
- These were activated (i.e., enlarged), and intensely immunoreactive, even in the fetal group.
Why it matters
This study found that people with Down's syndrome have about twice as many astrocytes overexpressing S100beta as controls across all ages examined. It suggests a possible role for S100beta in plaque formation, but it is an observational study and does not test any treatment or prevention.
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Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| Journal's citation record | 3 / 4 | Neurobiology of Aging: journal h-index 263 (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 | 1998 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 134 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.5 citations a year over 30 year(s) since 1998 |
| Impact for its field and year | 3 / 6 | Cited 4.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 14 other studies in this library |
| Still being cited | 1 / 4 | Cited 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Robert Emil Mrak: h-index 60 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Stanford University: institution h-index 2,684 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 4 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9880042) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/s0197-4580(98)00074-8
- PubMed: 9880042
- 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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