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Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation
Wolozin B, Iwasaki K, Vito P, Ganjei JK, Lacanà E, Sunderland T, Zhao B, Kusiak JW et al.. Science (New York, N.Y.), 1996-12-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells. The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved.
What this study adds
Evidence grade: Low
In PC12 cells, overexpression of presenilin 2 increased apoptosis, and a familial Alzheimer's disease mutation in PS2 produced a molecule with enhanced basal apoptotic activity. This is a cell study, so it does not show any treatment, cure, or prevention for 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
Wolozin, B., Iwasaki, K., Vito, P., Ganjei, J. K., Lacanà, E., Sunderland, T., et al. (1996). Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation. Science (New York, N.Y.). https://doi.org/10.1126/science.274.5293.1710
Vancouver
Wolozin B, Iwasaki K, Vito P, Ganjei JK, Lacanà E, Sunderland T, et al. Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation. Science (New York, N.Y.). 1996. doi:10.1126/science.274.5293.1710. PMID: 8939861.
BibTeX
@article{wolozin1996-8939861,
author = {Wolozin, B. and Iwasaki, K. and Vito, P. and Ganjei, J. K. and Lacanà, E. and Sunderland, T. and Zhao, B. and Kusiak, J. W. and others},
title = {{Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation}},
journal = {Science (New York, N.Y.)},
year = {1996},
doi = {10.1126/science.274.5293.1710},
pmid = {8939861},
url = {https://doi.org/10.1126/science.274.5293.1710}
}
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
- Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells.
- The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved.
- A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity.
- This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease.
Why it matters
In PC12 cells, overexpression of presenilin 2 increased apoptosis, and a familial Alzheimer's disease mutation in PS2 produced a molecule with enhanced basal apoptotic activity. This is a cell study, so it does not show any treatment, cure, or prevention for Alzheimer's disease in people.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 53/100
Published in a top-tier 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 | 10 / 10 | Tier 1 — top-tier general journal (Science (New York, N.Y.)) |
| Journal's citation record | 4 / 4 | Science: journal h-index 1,754 (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 | 1996 — 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 | 6 / 7 | Cited 423 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.2 citations a year over 32 year(s) since 1996 |
| Impact for its field and year | 5 / 6 | Cited 34.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Luciano D'adamio: h-index 54 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8939861) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
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