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Superoxide dismutase SOD1, encoded on chromosome 21, but not SOD2 is overexpressed in brains of patients with Down syndrome
Gulesserian T, Seidl R, Hardmeier R, Cairns N, Lubec G.. Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2001-01-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Background The antioxidant enzyme Cu/Zn-superoxide dismutase-1 (SOD1) gene is localized to chromosome 21q22.1 and catalyzes the dismutation of superoxide anions to hydrogen peroxide, which may lead to the increased production of active oxygen species in Down Syndrome (DS), trisomy 21. Although a number of studies have addressed this question, proposing the overexpression hypothesis, no specific protein-chemical data on SOD protein levels in the brains of patients with DS are available. Methods We therefore determined the protein SOD-1 and SOD-2 levels in the brains of controls (n = 9) and adult patients with DS (n = 9) and Alzheimer disease (AD; n = 9). Two-dimensional electrophoresis followed by matrix-assisted laser desorption/ionization-mass spectroscopy detection and identification was used for the analyses. Results We found significantly increased SOD-1 levels in DS temporal, parietal, and occipital cortex, whereas SOD-1 was decreased in the AD temporal cortex and SOD-2 was comparable between all groups. Conclusions Increased SOD-1 levels in patients with DS may reflect the overexpression by the trisomic state, as a response to the oxidative stress, as has been proposed in DS by several authors. However, it well may be that glial proliferation, which is markedly increased in DS brain, may underlie the increased brain levels of this ubiquitous protein. The decrease of SOD1 in the temporal cortex of patients with AD may reflect an antiapoptotic mechanism or simply cell loss in the brain.
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APA 7th
Gulesserian, T., Seidl, R., Hardmeier, R., Cairns, N., & Lubec, G. (2001). Superoxide dismutase SOD1, encoded on chromosome 21, but not SOD2 is overexpressed in brains of patients with Down syndrome. Journal of investigative medicine : the official publication of the American Federation for Clinical Research. https://doi.org/10.2310/6650.2001.34089
Vancouver
Gulesserian T, Seidl R, Hardmeier R, Cairns N, Lubec G. Superoxide dismutase SOD1, encoded on chromosome 21, but not SOD2 is overexpressed in brains of patients with Down syndrome. Journal of investigative medicine : the official publication of the American Federation for Clinical Research. 2001. doi:10.2310/6650.2001.34089. PMID: 11217146.
BibTeX
@article{gulesserian2001-11217146,
author = {Gulesserian, T. and Seidl, R. and Hardmeier, R. and Cairns, N. and Lubec, G.},
title = {{Superoxide dismutase SOD1, encoded on chromosome 21, but not SOD2 is overexpressed in brains of patients with Down syndrome}},
journal = {Journal of investigative medicine : the official publication of the American Federation for Clinical Research},
year = {2001},
doi = {10.2310/6650.2001.34089},
pmid = {11217146},
url = {https://doi.org/10.2310/6650.2001.34089}
}
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Key findings
- Results We found significantly increased SOD-1 levels in DS temporal, parietal, and occipital cortex, whereas SOD-1 was decreased in the AD temporal cortex and SOD-2 was comparable between all groups.
Why it matters
In brain tissue from 9 controls, 9 adults with Down syndrome and 9 with Alzheimer's disease, SOD-1 levels were significantly increased in Down syndrome temporal, parietal and occipital cortex, decreased in Alzheimer's disease temporal cortex, and SOD-2 was comparable between all groups. The authors note the increase may reflect the trisomic state, oxidative stress, or increased glial proliferation.
Study details
- Evidence strengthLow
How this study scored 40/100
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 (Journal of investigative medicine : the official publication of the American Federation for Clinical Research) |
| Journal's citation record | 1 / 4 | Journal of Investigative Medicine: journal h-index 88 (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 | 2001 — 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 | 4 / 7 | Cited 92 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.4 citations a year over 27 year(s) since 2001 |
| Impact for its field and year | 3 / 6 | Cited 5.2× 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 | 2 / 4 | Cited 15 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Gert Lübec: h-index 70 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | King's College London: institution h-index 1,348 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 11217146) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 40 / 100 | — |
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