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Statins reduce amyloid-beta production through inhibition of protein isoprenylation
Ostrowski SM, Wilkinson BL, Golde TE, Landreth G.. The Journal of biological chemistry, 2007-07-23
Topic: Brain proteins, microglia and lab models
Plain-language summary
Epidemiological evidence suggests that long term treatment with hydroxymethylglutaryl-CoA reductase inhibitors, or statins, decreases the risk for developing Alzheimer disease (AD). However, statin-mediated AD protection cannot be fully explained by reduction of cholesterol levels. In addition to their cholesterol lowering effects, statins have pleiotropic actions and act to lower the concentrations of isoprenoid intermediates, such as geranylgeranyl pyrophosphate and farnesyl pyrophosphate.
What this study adds
Evidence grade: Low
This cell study found that statins reduced amyloid-beta production through inhibition of protein isoprenylation, not just through cholesterol lowering. It is laboratory work on a possible mechanism and does not show that statins treat or prevent Alzheimer's disease.
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
Ostrowski, S. M., Wilkinson, B. L., Golde, T. E., & Landreth, G. (2007). Statins reduce amyloid-beta production through inhibition of protein isoprenylation. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m702640200
Vancouver
Ostrowski SM, Wilkinson BL, Golde TE, Landreth G. Statins reduce amyloid-beta production through inhibition of protein isoprenylation. The Journal of biological chemistry. 2007. doi:10.1074/jbc.m702640200. PMID: 17646164.
BibTeX
@article{ostrowski2007-17646164,
author = {Ostrowski, S. M. and Wilkinson, B. L. and Golde, T. E. and Landreth, G.},
title = {{Statins reduce amyloid-beta production through inhibition of protein isoprenylation}},
journal = {The Journal of biological chemistry},
year = {2007},
doi = {10.1074/jbc.m702640200},
pmid = {17646164},
url = {https://doi.org/10.1074/jbc.m702640200}
}
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
- However, statin-mediated AD protection cannot be fully explained by reduction of cholesterol levels.
- In addition to their cholesterol lowering effects, statins have pleiotropic actions and act to lower the concentrations of isoprenoid intermediates, such as geranylgeranyl pyrophosphate and farnesyl pyrophosphate.
- The Rho and Rab family small G-proteins require addition of these isoprenyl moieties at their C termini for normal GTPase function.
- In neuroblastoma cell lines, treatment with statins inhibits the membrane localization of Rho and Rab proteins at statin doses as low as 200 nm, without affecting cellular cholesterol levels.
Why it matters
This cell study found that statins reduced amyloid-beta production through inhibition of protein isoprenylation, not just through cholesterol lowering. It is laboratory work on a possible mechanism and does not show that statins treat or prevent Alzheimer's disease.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of biological chemistry) |
| Journal's citation record | 4 / 4 | Journal of Biological Chemistry: journal h-index 780 (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 | 2007 — within 20 year(s) of the newest study here |
| 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 | 5 / 7 | Cited 182 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.7 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 4 / 6 | Cited 10.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 1 / 4 | Cited 11 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Gary E. Landreth: h-index 101 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17646164) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1074/jbc.m702640200
- PubMed: 17646164
- Original source →
- Free full text: Journal of Biological Chemistry →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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