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Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain
Butterfield DA, Boyd-Kimball D.. Brain pathology (Zurich, Switzerland), 2004-10-01
Topic: Amyloid, tau and blood-test diagnosis
Oxidative stress is extensive in Alzheimer disease (AD) brain. Amyloid beta-peptide (1-42) has been shown to induce oxidative stress and neurotoxicity in vitro and in vivo. Genetic mutations that result in increased production of Abeta1-42 from amyloid precursor protein are associated with an early onset and accelerated pathology of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Butterfield, D. A., & Boyd-Kimball, D. (2004). Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain. Brain pathology (Zurich, Switzerland). https://doi.org/10.1111/j.1750-3639.2004.tb00087.x
Vancouver
Butterfield DA, Boyd-Kimball D. Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain. Brain pathology (Zurich, Switzerland). 2004. doi:10.1111/j.1750-3639.2004.tb00087.x. PMID: 15605990.
BibTeX
@article{butterfield2004-15605990,
author = {Butterfield, D. A. and Boyd-Kimball, D.},
title = {{Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain}},
journal = {Brain pathology (Zurich, Switzerland)},
year = {2004},
doi = {10.1111/j.1750-3639.2004.tb00087.x},
pmid = {15605990},
url = {https://doi.org/10.1111/j.1750-3639.2004.tb00087.x}
}
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
- Amyloid beta-peptide (1-42) has been shown to induce oxidative stress and neurotoxicity in vitro and in vivo.
- Genetic mutations that result in increased production of Abeta1-42 from amyloid precursor protein are associated with an early onset and accelerated pathology of AD.
- Consequently, Abeta1-42 has been proposed to play a central role in the pathogenesis of AD as a mediator of oxidative stress.
- In this review, we discuss the role of Abeta1-42 in the lipid peroxidation and protein oxidation evident in AD brain and the implications of such oxidative stress for the function of various proteins that we have identified as specifically oxidized in AD brain compared to control, using proteomics methods.
Why it matters
This review discusses evidence that amyloid beta-peptide(1-42) causes oxidative stress and neurotoxicity and that mutations increasing its production lead to early-onset Alzheimer's disease. It proposes a central role for this peptide in disease but reports no treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 41/100
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 (Brain pathology (Zurich, Switzerland)) |
| Journal's citation record | 2 / 4 | Brain Pathology: journal h-index 183 (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 | 2004 — 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 | 5 / 7 | Cited 262 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 10.9 citations a year over 24 year(s) since 2004 |
| Impact for its field and year | 3 / 6 | Cited 7.1× 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 | 2 / 4 | Cited 27 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Debra Boyd‐Kimball: h-index 23 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Kentucky: institution h-index 824 (OpenAlex) |
| Multicenter 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 15605990) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/j.1750-3639.2004.tb00087.x
- PubMed: 15605990
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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