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S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques
Sheng JG, Mrak RE, Griffin WS.. Journal of neuroscience research, 1994-11-01
Topic: Amyloid, tau and blood-test diagnosis
Increased synthesis and release of S100 beta protein from activated astrocytes has been implicated in the overgrowth of dystrophic neurites in neuritic plaques in Alzheimer disease (AD). To evaluate the quantitative relationships between tissues levels of S100 beta and the numbers of neuritic plaques in AD patients, we counted neuritic plaques, by Tau-2 immunoreactive (Tau-2+) labeling, in tissue sections of hippocampus and adjacent temporal cortex and measured the levels of S100 beta protein, by Western immunoblot labeling, in samples of analogous regions from contralateral hemisphere of the same patients. In AD, tissue levels of S100 beta (two- to fivefold that of controls) were significantly correlated with the number of Tau-2+ plaques (R = 0.82, P < .01). Dual-label immunohistochemical analysis showed that most S100 beta+ cells were activated GFAP+ astrocytes. These results were substantiated by a significant correlation between S100 beta and GFAP tissue levels (R = 0.81, P < .05). Many of the S100 beta+ astrocytes were clustered around and within Tau-2+ plaques. Indeed, no Tau-2+ plaques were found without associated activated S100 beta+ astrocytes. Our findings provide further evidence of a role for S100 beta protein in dysregulation of neurons that leads to apparently nonsensical growth of imperfect neurites in AD, a potential key element in early stages of neuritic plaque pathogenesis.
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APA 7th
Sheng, J. G., Mrak, R. E., & Griffin, W. S. (1994). S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques. Journal of neuroscience research. https://doi.org/10.1002/jnr.490390406
Vancouver
Sheng JG, Mrak RE, Griffin WS. S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques. Journal of neuroscience research. 1994. doi:10.1002/jnr.490390406. PMID: 7884819.
BibTeX
@article{sheng1994-7884819,
author = {Sheng, J. G. and Mrak, R. E. and Griffin, W. S.},
title = {{S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques}},
journal = {Journal of neuroscience research},
year = {1994},
doi = {10.1002/jnr.490390406},
pmid = {7884819},
url = {https://doi.org/10.1002/jnr.490390406}
}
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Key findings
- In AD, tissue levels of S100 beta (two- to fivefold that of controls) were significantly correlated with the number of Tau-2+ plaques (R = 0.82, P < .01).
- Dual-label immunohistochemical analysis showed that most S100 beta+ cells were activated GFAP+ astrocytes.
- These results were substantiated by a significant correlation between S100 beta and GFAP tissue levels (R = 0.81, P < .05).
- Our findings provide further evidence of a role for S100 beta protein in dysregulation of neurons that leads to apparently nonsensical growth of imperfect neurites in AD, a potential key element in early stages of neuritic plaque pathogenesis.
Why it matters
In brain tissue from Alzheimer patients, higher levels of S100 beta protein correlated with the number of neuritic plaques and with GFAP levels. This suggests a possible role for S100 beta in plaque formation but reports no treatment, cure or prevention.
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Study details
- Evidence strengthLow
How this study scored 41/100
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 (Journal of neuroscience research) |
| Journal's citation record | 2 / 4 | Journal of Neuroscience Research: journal h-index 222 (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 | 1994 — 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 186 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.5 citations a year over 34 year(s) since 1994 |
| Impact for its field and year | 3 / 6 | Cited 5.5× 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 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author W. Sue T. Griffin: h-index 66 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University of Arkansas for Medical Sciences: institution h-index 591 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 7884819) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
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