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Oxidized cholesterol as the driving force behind the development of Alzheimer's disease
Gamba P, Testa G, Gargiulo S, Staurenghi E, Poli G, Leonarduzzi G.. Frontiers in aging neuroscience, 2015-06-19
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD), the most common neurodegenerative disorder associated with dementia, is typified by the pathological accumulation of amyloid Aβ peptides and neurofibrillary tangles (NFT) within the brain. Considerable evidence indicates that many events contribute to AD progression, including oxidative stress, inflammation, and altered cholesterol metabolism. The brain's high lipid content makes it particularly vulnerable to oxidative species, with the consequent enhancement of lipid peroxidation and cholesterol oxidation, and the subsequent formation of end products, mainly 4-hydroxynonenal and oxysterols, respectively from the two processes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gamba, P., Testa, G., Gargiulo, S., Staurenghi, E., Poli, G., & Leonarduzzi, G. (2015). Oxidized cholesterol as the driving force behind the development of Alzheimer's disease. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2015.00119
Vancouver
Gamba P, Testa G, Gargiulo S, Staurenghi E, Poli G, Leonarduzzi G. Oxidized cholesterol as the driving force behind the development of Alzheimer's disease. Frontiers in aging neuroscience. 2015. doi:10.3389/fnagi.2015.00119. PMID: 26150787.
BibTeX
@article{gamba2015-26150787,
author = {Gamba, P. and Testa, G. and Gargiulo, S. and Staurenghi, E. and Poli, G. and Leonarduzzi, G.},
title = {{Oxidized cholesterol as the driving force behind the development of Alzheimer's disease}},
journal = {Frontiers in aging neuroscience},
year = {2015},
doi = {10.3389/fnagi.2015.00119},
pmid = {26150787},
url = {https://doi.org/10.3389/fnagi.2015.00119}
}
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
- Considerable evidence indicates that many events contribute to AD progression, including oxidative stress, inflammation, and altered cholesterol metabolism.
- The brain's high lipid content makes it particularly vulnerable to oxidative species, with the consequent enhancement of lipid peroxidation and cholesterol oxidation, and the subsequent formation of end products, mainly 4-hydroxynonenal and oxysterols, respectively from the two processes.
- The chronic inflammatory events observed in the AD brain include activation of microglia and astrocytes, together with enhancement of inflammatory molecule and free radical release.
- Along with glial cells, neurons themselves have been found to contribute to neuroinflammation in the AD brain, by serving as sources of inflammatory mediators.
Why it matters
This paper proposes that oxidative stress, inflammation and altered cholesterol metabolism contribute to Alzheimer's disease progression, with lipid peroxidation and cholesterol oxidation forming products such as 4-hydroxynonenal and oxysterols. It presents a proposed mechanism rather than evidence that targeting cholesterol oxidation treats or prevents the disease.
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Aging Neuroscience: journal h-index 174 (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 | 2015 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 202 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.5 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 4 / 6 | Cited 11.0× 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 48 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Gabriella Leonarduzzi: h-index 52 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Turin: institution h-index 903 (OpenAlex) |
| Multi-centre 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 26150787) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnagi.2015.00119
- PubMed: 26150787
- Original source →
- Free full text: Frontiers in Aging Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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