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Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration
Keeney JT, Swomley AM, Förster S, Harris JL, Sultana R, Butterfield DA.. Proteomics. Clinical applications, 2013-01-01
Topic: Brain proteins, microglia and lab models
Proteomics has a wide range of applications, including determination of differences in the proteome in terms of expression and post-translational protein modifications. Redox proteomics allows the identification of specific targets of protein oxidation in a biological sample. Using proteomic techniques, apolipoprotein A-I (ApoA-I) has been found at decreased levels in subjects with a variety of neurodegenerative disorders including in the serum and cerebrospinal fluid (CSF) of Alzheimer disease (AD), Parkinson disease (PD), and Down syndrome (DS) with gout subjects. ApoA-I plays roles in cholesterol transport and regulation of inflammation. Redox proteomics further showed ApoA-I to be highly oxidatively modified and particularly susceptible to modification by 4-hydroxy-2-trans-nonenal (HNE), a lipid peroxidation product. In the current review, we discuss the consequences of oxidation of ApoA-I in terms of neurodegeneration. ROS-associated chemotherapy related ApoA-I oxidation leads to elevation of peripheral levels of tumor necrosis factor-α (TNF-α) that can cross the blood-brain barrier (BBB) causing a signaling cascade that can contribute to neuronal death, likely a contributor to what patients refer to as "chemobrain." Current evidence suggests ApoA-I to be a promising diagnostic marker as well as a potential target for therapeutic strategies in these neurodegenerative disorders.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Keeney, J. T., Swomley, A. M., Förster, S., Harris, J. L., Sultana, R., & Butterfield, D. A. (2013). Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration. Proteomics. Clinical applications. https://doi.org/10.1002/prca.201200087
Vancouver
Keeney JT, Swomley AM, Förster S, Harris JL, Sultana R, Butterfield DA. Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration. Proteomics. Clinical applications. 2013. doi:10.1002/prca.201200087. PMID: 23027708.
BibTeX
@article{keeney2013-23027708,
author = {Keeney, J. T. and Swomley, A. M. and Förster, S. and Harris, J. L. and Sultana, R. and Butterfield, D. A.},
title = {{Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration}},
journal = {Proteomics. Clinical applications},
year = {2013},
doi = {10.1002/prca.201200087},
pmid = {23027708},
url = {https://doi.org/10.1002/prca.201200087}
}
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Key findings
- Using proteomic techniques, apolipoprotein A-I (ApoA-I) has been found at decreased levels in subjects with a variety of neurodegenerative disorders including in the serum and cerebrospinal fluid (CSF) of Alzheimer disease (AD), Parkinson disease (PD), and Down syndrome (DS) with gout subjects.
- ApoA-I plays roles in cholesterol transport and regulation of inflammation.
- Redox proteomics further showed ApoA-I to be highly oxidatively modified and particularly susceptible to modification by 4-hydroxy-2-trans-nonenal (HNE), a lipid peroxidation product.
- In the current review, we discuss the consequences of oxidation of ApoA-I in terms of neurodegeneration.
- ROS-associated chemotherapy related ApoA-I oxidation leads to elevation of peripheral levels of tumor necrosis factor-α (TNF-α) that can cross the blood-brain barrier (BBB) causing a signaling cascade that can contribute to neuronal death, likely a contributor to what patients refer to as "chemobrain."
Why it matters
This review reports that apolipoprotein A-I levels are decreased and the protein is highly oxidatively modified in serum and cerebrospinal fluid of people with Alzheimer's disease, Parkinson's disease, and Down syndrome with gout. It suggests ApoA-I may be a diagnostic marker and potential therapeutic target, but no treatment is tested.
Study details
- Evidence strengthLow
How this study scored 36/100
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 (Proteomics. Clinical applications) |
| Journal's citation record | 0 / 4 | PROTEOMICS - CLINICAL APPLICATIONS: journal h-index 74 (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 | 2013 — 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 | 4 / 7 | Cited 72 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.8 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 2 / 6 | Cited 2.9× 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 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author David Allan Butterfield: h-index 135 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Bonn: institution h-index 1,072 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23027708) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
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