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Antioxidants in Down syndrome
Lott IT.. Biochimica et biophysica acta, 2011-12-21
Topic: Brain proteins, microglia and lab models
Individuals with Down syndrome (DS) have high levels of oxidative stress throughout the lifespan. Mouse models of DS share some structural and functional abnormalities that parallel findings seen in the human phenotype. Several of the mouse models show evidence of cellular oxidative stress and have provided a platform for antioxidant intervention. Genes that are overexpressed on chromosome 21 are associated with oxidative stress and neuronal apoptosis. The lack of balance in the metabolism of free radicals generated during processes related to oxidative stress may have a direct role in producing the neuropathology of DS including the tendency to Alzheimer disease (AD). Mitochondria are often a target for oxidative stress and are considered to be a trigger for the onset of the AD process in DS. Biomarkers for oxidative stress have been described in DS and in AD in the general population. However, intervention trials using standard antioxidant supplements or diets have failed to produce uniform therapeutic effect. This chapter will examine the biological role of oxidative stress in DS and its relationship to abnormalities in both development and aging within the disorder. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease.
Key findings
- Genes that are overexpressed on chromosome 21 are associated with oxidative stress and neuronal apoptosis.
Why it matters
People with Down syndrome have high oxidative stress throughout life, and this review links that to extra copies of chromosome-21 genes and to mitochondrial damage that is "considered to be a trigger" for Alzheimer's changes in Down syndrome. That link is a working idea, not a proven cause. For families, the key point is that trials of standard antioxidant supplements or diets "have failed to produce uniform therapeutic effect," so this review does not support using them to protect against Alzheimer's.
Study details
- Evidence strengthLow
How this study scored 39/100
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. We have no data on journal's citation record, so that was left out: it earned 37 of the 96 points we could judge it on, which is 39 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biochimica et biophysica acta) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2012 — 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 83 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.2 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 3 / 6 | Cited 4.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 8 other studies in this library |
| Still being cited | 1 / 4 | Cited 8 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ira T. Lott: h-index 58 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of California, Irvine: institution h-index 1,195 (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 22206998) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 37 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 37 of the 96 points we could judge it on is 39 out of 100. |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.bbadis.2011.12.010
- PubMed: 22206998
- Original source →
- Free full text: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Lott, I. T. (2012). Antioxidants in Down syndrome. Biochimica et biophysica acta. https://doi.org/10.1016/j.bbadis.2011.12.010
Vancouver
Lott IT. Antioxidants in Down syndrome. Biochimica et biophysica acta. 2012. doi:10.1016/j.bbadis.2011.12.010. PMID: 22206998.
BibTeX
@article{lott2012-22206998,
author = {Lott, I. T.},
title = {{Antioxidants in Down syndrome}},
journal = {Biochimica et biophysica acta},
year = {2012},
doi = {10.1016/j.bbadis.2011.12.010},
pmid = {22206998},
url = {https://doi.org/10.1016/j.bbadis.2011.12.010}
}
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