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Astrocytic pathology of methionine sulfoximine-induced encephalopathy
Yamamoto T, Iwasaki Y, Sato Y, Yamamoto H, Konno H.. Acta neuropathologica, 1989-01-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
To investigate the roles imposed on astrocytes for glutamate metabolism, a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSO), was repeatedly administered to rats and histopathological changes were correlated with glycogen accumulation and the immunocytochemistry of GS and glial fibrillary acidic protein (GFAP). Prolonged MSO-loading (every 12 h up to three times, 100-150 mg/kg body weight) brought about the appearance of astrocytes with swollen, watery nuclei reminiscent of Alzheimer II glia chiefly in the neocortex, hippocampus and lateral thalamus after 24 h. Concomitantly, profound accumulation of glycogen ensued in the superficial three layers of the neocortex, hippocampus and pyriform cortex. GS immunoreactivity appeared enhanced in the cortex, hippocampus and lateral thalamus with parallel increase in GFAP immunoreactivity after prolonged treatment. Oligodendrocytes in the diencephalon and brain stem also normally contained GS immunoreactivity. Some animals developed necrotic lesions in the dorsolateral neocortex. The area of glycogen accumulation coincided with the known distribution of N-methyl D-aspartate (NMDA) glutamate receptors and, thus, GS may play important roles in NMDA receptor-mediated glutamate metabolism. The Alzheimer II type changes, however, did not correlate with NMDA-receptor distribution. These results indicate certain regionalizations in the roles of astrocytes and oligodendrocytes in glutamate and ammonia metabolisms.
What this study adds
Evidence grade: Low
In rats, repeated doses of a chemical that blocks glutamine synthetase caused astrocytes to swell and glycogen to build up in certain brain regions, along with changes in GS and GFAP. This is an animal study from 1989 and does not test any treatment, cure or prevention of Alzheimer's disease in people.
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
Yamamoto, T., Iwasaki, Y., Sato, Y., Yamamoto, H., & Konno, H. (1989). Astrocytic pathology of methionine sulfoximine-induced encephalopathy. Acta neuropathologica. https://doi.org/10.1007/bf00687370
Vancouver
Yamamoto T, Iwasaki Y, Sato Y, Yamamoto H, Konno H. Astrocytic pathology of methionine sulfoximine-induced encephalopathy. Acta neuropathologica. 1989. doi:10.1007/bf00687370. PMID: 2565645.
BibTeX
@article{yamamoto1989-2565645,
author = {Yamamoto, T. and Iwasaki, Y. and Sato, Y. and Yamamoto, H. and Konno, H.},
title = {{Astrocytic pathology of methionine sulfoximine-induced encephalopathy}},
journal = {Acta neuropathologica},
year = {1989},
doi = {10.1007/bf00687370},
pmid = {2565645},
url = {https://doi.org/10.1007/bf00687370}
}
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.
Key findings
- These results indicate certain regionalizations in the roles of astrocytes and oligodendrocytes in glutamate and ammonia metabolisms.
Why it matters
In rats, repeated doses of a chemical that blocks glutamine synthetase caused astrocytes to swell and glycogen to build up in certain brain regions, along with changes in GS and GFAP. This is an animal study from 1989 and does not test any treatment, cure or prevention of Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 34/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 1989 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 32 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.8 citations a year over 39 year(s) since 1989 |
| Impact for its field and year | 2 / 6 | Cited 1.0× 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 | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Hidehiko Konno: h-index 36 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Tohoku University: institution h-index 880 (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 2565645) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 34 / 100 | — |
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