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Enhanced GFAP expression in astrocytes of transgenic mice expressing the human brain-specific trypsinogen IV
Minn A, Schubert M, Neiss WF, Müller-Hill B.. Glia, 1998-04-01
Topic: Brain proteins, microglia and lab models
We recently identified a cDNA encoding a human brain specific trypsinogen (trypsinogen IV). In order to test whether trypsinogen IV is involved in CNS diseases of, or injury response in, mammalian brain, a mouse model was developed in which the human trypsinogen IV was expressed specifically in neurons. Immunocytochemical analysis of the brains of transgenic mice revealed a striking enhancement of glial fibrillar acidic protein (GFAP) expression in astrocytes. This remarkable astrocytic reaction was detected in the brains of mice as young as 2 months and did not diminish in the older animals we tested. However, we did not find gross evidence for neurodegeneration, nor for reactive microglial cells. The long-term survival of these animals should provide a model with which to study the mechanism of nerve-astroglia interactions. In addition, the possible participation of trypsin IV in the metabolism of the Alzheimer precursor protein (APP) was investigated by immunostaining brains from transgenic mice with beta-amyloid (betaA4) antibodies. Immunocytochemical staining of brains from one year old transgenic mice revealed an intense intracellular betaA4-like signal in neurons.
Key findings
- Immunocytochemical analysis of the brains of transgenic mice revealed a striking enhancement of glial fibrillar acidic protein (GFAP) expression in astrocytes.
- Immunocytochemical staining of brains from one year old transgenic mice revealed an intense intracellular betaA4-like signal in neurons.
Why it matters
In transgenic mice expressing human brain-specific trypsinogen IV, astrocytes showed increased GFAP expression and one-year-old mice showed an intracellular beta-amyloid-like signal in neurons. This is an animal study from 1998 and does not demonstrate any treatment or prevention for Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 32/100
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 (Glia) |
| Journal's citation record | 2 / 4 | Glia: journal h-index 233 (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 | Laboratory or animal study (title names “transgenic”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 39 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.3 citations a year over 30 year(s) since 1998 |
| Impact for its field and year | 1 / 6 | Cited 0.8× 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 | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Benno Müller‐Hill: h-index 57 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Cologne: institution h-index 879 (OpenAlex) |
| Multi-centre 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 9517566) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 32 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1002/(sici)1098-1136(199804)22:4<338::aid-glia3>3.0.co;2-#
- PubMed: 9517566
- Original source →
May need a subscription Unpaywall, Europe PMC and OpenAlex found no free copy of the full text (checked 10 Oct 2026), so the publisher may charge for it. The PubMed abstract is free.
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
Minn, A., Schubert, M., Neiss, W. F., & Müller-Hill, B. (1998). Enhanced GFAP expression in astrocytes of transgenic mice expressing the human brain-specific trypsinogen IV. Glia. https://doi.org/10.1002/(sici)1098-1136(199804)22:4<338::aid-glia3>3.0.co;2-#
Vancouver
Minn A, Schubert M, Neiss WF, Müller-Hill B. Enhanced GFAP expression in astrocytes of transgenic mice expressing the human brain-specific trypsinogen IV. Glia. 1998. doi:10.1002/(sici)1098-1136(199804)22:4<338::aid-glia3>3.0.co;2-#. PMID: 9517566.
BibTeX
@article{minn1998-9517566,
author = {Minn, A. and Schubert, M. and Neiss, W. F. and Müller-Hill, B.},
title = {{Enhanced GFAP expression in astrocytes of transgenic mice expressing the human brain-specific trypsinogen IV}},
journal = {Glia},
year = {1998},
doi = {10.1002/(sici)1098-1136(199804)22:4<338::aid-glia3>3.0.co;2-#},
pmid = {9517566},
url = {https://doi.org/10.1002/(sici)1098-1136(199804)22:4<338::aid-glia3>3.0.co;2-#}
}
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