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Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle
Askanas V, McFerrin J, Baqué S, Alvarez RB, Sarkozi E, Engel WK.. Proceedings of the National Academy of Sciences of the United States of America, 1996-02-01
Topic: Brain proteins, microglia and lab models
As in Alzheimer-disease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751 mRNA. Other similarities between IBM muscle and AD brain phenotypes include paired helical filaments, hyperphosphorylated tau protein, apolipoprotein E, and mitochondrial abnormalities, including decreased cytochrome-c oxidase (COX) activity. The pathogenesis of these abnormalities in IBM muscle and AD brain is not known.
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APA 7th
Askanas, V., McFerrin, J., Baqué, S., Alvarez, R. B., Sarkozi, E., & Engel, W. K. (1996). Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.93.3.1314
Vancouver
Askanas V, McFerrin J, Baqué S, Alvarez RB, Sarkozi E, Engel WK. Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle. Proceedings of the National Academy of Sciences of the United States of America. 1996. doi:10.1073/pnas.93.3.1314. PMID: 8577761.
BibTeX
@article{askanas1996-8577761,
author = {Askanas, V. and McFerrin, J. and Baqué, S. and Alvarez, R. B. and Sarkozi, E. and Engel, W. K.},
title = {{Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {1996},
doi = {10.1073/pnas.93.3.1314},
pmid = {8577761},
url = {https://doi.org/10.1073/pnas.93.3.1314}
}
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Key findings
- Other similarities between IBM muscle and AD brain phenotypes include paired helical filaments, hyperphosphorylated tau protein, apolipoprotein E, and mitochondrial abnormalities, including decreased cytochrome-c oxidase (COX) activity.
- The pathogenesis of these abnormalities in IBM muscle and AD brain is not known.
- We now report that direct transfer of the beta APP gene, using adenovirus vector, into cultured normal human muscle fibers causes structural abnormalities of mitochondria and decreased COX activity.
- In this adenovirus-mediated beta APP gene transfer, we demonstrated that beta APP overproduction can induce mitochondrial abnormalities.
Why it matters
This laboratory study found that inserting the beta-amyloid precursor protein gene into cultured normal human muscle fibers caused mitochondrial abnormalities. This is early cell-based work and does not show that the same process happens in Alzheimer's disease or that it can be treated.
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Study details
- Evidence strengthLow
How this study scored 42/100
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 (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 | 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 | Laboratory or animal study (title names “cultured”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 140 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.4 citations a year over 32 year(s) since 1996 |
| Impact for its field and year | 3 / 6 | Cited 4.1× 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 | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author W. King Engel: h-index 55 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Southern California: institution h-index 1,521 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8577761) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
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