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Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease: a potential molecular basis for neuronal degeneration
Saito K, Elce JS, Hamos JE, Nixon RA.. Proceedings of the National Academy of Sciences of the United States of America, 1993-04-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Calcium-activated neutral proteinases (CANPs or calpains) are believed to be key enzymes in intracellular signaling cascades and potential mediators of calcium-induced neuronal degeneration. To investigate their involvement in Alzheimer disease, we identified three isoforms of muCANP (calpain I) in human postmortem brain corresponding to an 80-kDa precursor and two autolytically activated isoforms (78 and 76 kDa). As an index of changes in the in vivo activity of muCANP in Alzheimer disease, the ratio of the 76-kDa activated isoform of muCANP to its 80-kDa precursor was measured by immunoassay in selected brain regions from 22 individuals with Alzheimer disease and 18 normal controls.
What this study adds
Evidence grade: Low
The record lists 22 participants. In postmortem brain tissue from people with Alzheimer's disease, this study found widespread activation of the calcium-activated proteinase calpain. This suggests calpain may be involved in neuronal degeneration, but it does not test any treatment.
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
Saito, K., Elce, J. S., Hamos, J. E., & Nixon, R. A. (1993). Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease: a potential molecular basis for neuronal degeneration. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.90.7.2628
Vancouver
Saito K, Elce JS, Hamos JE, Nixon RA. Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease: a potential molecular basis for neuronal degeneration. Proceedings of the National Academy of Sciences of the United States of America. 1993. doi:10.1073/pnas.90.7.2628. PMID: 8464868.
BibTeX
@article{saito1993-8464868,
author = {Saito, K. and Elce, J. S. and Hamos, J. E. and Nixon, R. A.},
title = {{Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease: a potential molecular basis for neuronal degeneration}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {1993},
doi = {10.1073/pnas.90.7.2628},
pmid = {8464868},
url = {https://doi.org/10.1073/pnas.90.7.2628}
}
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
- To investigate their involvement in Alzheimer disease, we identified three isoforms of muCANP (calpain I) in human postmortem brain corresponding to an 80-kDa precursor and two autolytically activated isoforms (78 and 76 kDa).
- As an index of changes in the in vivo activity of muCANP in Alzheimer disease, the ratio of the 76-kDa activated isoform of muCANP to its 80-kDa precursor was measured by immunoassay in selected brain regions from 22 individuals with Alzheimer disease and 18 normal controls.
- This muCANP activation ratio was elevated 3-fold in the prefrontal cortex from patients with Alzheimer disease but not from patients with Huntington disease.
- The activation ratio was also significantly elevated, but to a lesser degree, in brain regions where Alzheimer pathology is milder and has not led to overt neuronal degeneration.
Why it matters
In postmortem brain tissue from people with Alzheimer's disease, this study found widespread activation of the calcium-activated proteinase calpain. This suggests calpain may be involved in neuronal degeneration, but it does not test any treatment.
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Study details
- Participants22
- Evidence strengthLow
How this study scored 51/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Proceedings of the National Academy of Sciences of the United States of America) |
| Journal's citation record | 4 / 4 | Proceedings of the National Academy of Sciences: journal h-index 1,167 (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 | 1993 — older than 20 years, still counted |
| Sample size | 1 / 4 | 22 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 583 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 16.7 citations a year over 35 year(s) since 1993 |
| Impact for its field and year | 3 / 6 | Cited 7.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Ralph A. Nixon: h-index 115 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Massachusetts Chan Medical School: institution h-index 990 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8464868) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
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