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Beta-amyloid, oxidative stress and down syndrome
Lott IT, Head E, Doran E, Busciglio J.. Current Alzheimer research, 2006-12-01
Topic: Brain proteins, microglia and lab models
Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD). Chromosome 21 contains several genes that have been implicated in neurodegenerative mechanisms. These include Cu/Zn superoxide dismutase (SOD-1), Ets-2 transcription factors, Down Syndrome Critical Region 1 (DSCR1) stress-inducible factor, and the amyloid precursor protein (APP). The accumulation of Abeta plaques is progressive across the lifespan in DS. Overexpression of APP in the obligate region for DS is associated with abundant Abeta plaques and tangles consistent with Braak stage V-VI. Intraneuronal Abeta in DS appears to trigger a pathological cascade leading to oxidative stress and a neurodegeneration typical of AD. There are suggestions that an increase in subcellular processing of APP and factors related to membrane APP cleavage favor the secretion of Abeta with age in DS. A misbalance between SOD-1 and glutathione perioxidase activity in DS has been linked to free radical generation. Ets-2 and DSCR1 overexpression in DS has been linked to cell degeneration. Age-related accumulation of somatic DNA mutations in both DS and AD contribute to oxidative stress that exacerbates the imbalance in gene expression. This leads to enhanced Abeta deposition and further neuronal vulnerability. The consequence of these factors and their temporal relationships is likely to be the subject of future research. Since the pathological processes leading to AD are seen across the lifespan in DS, an opportunity is afforded for early pharmacological intervention in the disorder.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Lott, I. T., Head, E., Doran, E., & Busciglio, J. (2006). Beta-amyloid, oxidative stress and down syndrome. Current Alzheimer research. https://doi.org/10.2174/156720506779025305
Vancouver
Lott IT, Head E, Doran E, Busciglio J. Beta-amyloid, oxidative stress and down syndrome. Current Alzheimer research. 2006. doi:10.2174/156720506779025305. PMID: 17168651.
BibTeX
@article{lott2006-17168651,
author = {Lott, I. T. and Head, E. and Doran, E. and Busciglio, J.},
title = {{Beta-amyloid, oxidative stress and down syndrome}},
journal = {Current Alzheimer research},
year = {2006},
doi = {10.2174/156720506779025305},
pmid = {17168651},
url = {https://doi.org/10.2174/156720506779025305}
}
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
- Overexpression of APP in the obligate region for DS is associated with abundant Abeta plaques and tangles consistent with Braak stage V-VI.
- There are suggestions that an increase in subcellular processing of APP and factors related to membrane APP cleavage favor the secretion of Abeta with age in DS.
Why it matters
This review describes how chromosome 21 genes including SOD-1 and APP contribute to amyloid beta plaque accumulation, oxidative stress, and neurodegeneration in Down syndrome. It is a mechanistic overview and reports no tested treatment, cure, or prevention.
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current Alzheimer research) |
| Journal's citation record | 1 / 4 | Current Alzheimer Research: journal h-index 119 (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 | 2006 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 110 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.0 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 3 / 6 | Cited 3.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 18 other studies in this library |
| Still being cited | 1 / 4 | Cited 7 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jorge A. Busciglio: h-index 46 (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 17168651) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
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