This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

50/100

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Oxidative stress is implicated in the pathogenesis and progression of Alzheimer's disease (AD) and its earlier stage, amnestic mild cognitive impairment (aMCI). One source of oxidative stress in AD and aMCI brains is that associated with amyloid-β peptide, Aβ1-42 oligomers. Our laboratory first showed in AD elevated oxidative stress occurred in brain regions rich in Aβ1-42, but not in Aβ1-42-poor regions, and was among the first to demonstrate Aβ peptides led to lipid peroxidation (indexed by HNE) in AD and aMCI brains. Oxidatively modified proteins have decreased function and contribute to damaged key biochemical and metabolic pathways in which these proteins normally play a role. Identification of oxidatively modified brain proteins by the methods of redox proteomics was pioneered in the Butterfield laboratory. Four recurring altered pathways secondary to oxidative damage in brain from persons with AD, aMCI, or Down syndrome with AD are interrelated and contribute to neuronal death. This "Quadrilateral of Neuronal Death" includes altered: glucose metabolism, mTOR activation, proteostasis network, and protein phosphorylation. Some of these pathways are altered even in brains of persons with preclinical AD. We opine that targeting these pathways pharmacologically and with lifestyle changes potentially may provide strategies to slow or perhaps one day, prevent, progression or development of this devastating dementing disorder. This invited review outlines both in vitro and in vivo studies from the Butterfield laboratory related to Aβ1-42 and AD and discusses the importance and implications of some of the major achievements of the Butterfield laboratory in AD research.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Butterfield, D. A., & Boyd-Kimball, D. (2018). Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease. Journal of Alzheimer's disease : JAD. https://doi.org/10.3233/jad-170543

Vancouver

Butterfield DA, Boyd-Kimball D. Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease. Journal of Alzheimer's disease : JAD. 2018. doi:10.3233/jad-170543. PMID: 29562527.

BibTeX

@article{butterfield2018-29562527,
  author  = {Butterfield, D. A. and Boyd-Kimball, D.},
  title   = {{Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease}},
  journal = {Journal of Alzheimer's disease : JAD},
  year    = {2018},
  doi     = {10.3233/jad-170543},
  pmid    = {29562527},
  url     = {https://doi.org/10.3233/jad-170543}
}

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

One source of oxidative stress in AD and aMCI brains is that associated with amyloid-β peptide, Aβ1-42 oligomers.

Why it matters

This invited review pulls together a single laboratory's work linking amyloid-β (Aβ1-42) oligomers to oxidative damage in the brains of people with Alzheimer's, its earlier stage amnestic MCI, and Down syndrome with AD. It groups the downstream damage into four interrelated pathways it calls the "Quadrilateral of Neuronal Death": glucose metabolism, mTOR activation, the proteostasis network and protein phosphorylation. It notes that some of these changes appear even in preclinical AD. The authors' suggestion that drugs or lifestyle changes aimed at these pathways might slow progression is stated as their opinion, not a tested result.

Study details

Evidence strengthLow

How this study scored 50/100

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 (Journal of Alzheimer's disease : JAD)
Journal's citation record	2 / 4	Journal of Alzheimer s Disease: journal h-index 218 (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	2 / 5	2018 — within 10 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	6 / 7	Cited 399 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	39.9 citations a year over 10 year(s) since 2018
Impact for its field and year	5 / 6	Cited 24.4× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 9 other studies in this library
Still being cited	3 / 4	Cited 126 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)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 29562527)
Free to read	2 / 2	Free to read
Total	50 / 100	—

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here. Showing 12 of 22.

Later studies that cite this one

9 studies in the alzhub library list this one in their references. Showing the 8 highest-scoring.

Related studies in Mild cognitive impairment

Also tagged “precursor”

1,339 studies in the library carry the topic tag “precursor”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 1,339 tagged studies.

Similar studies

More on Mild cognitive impairment

See all studies in Mild cognitive impairment →