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47/100

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Down syndrome and Alzheimer's

Topic: Brain proteins, microglia and lab models

Down syndrome (DS) is the most common genetic cause of intellectual disability in children, and the number of adults with DS reaching old age is increasing. By the age of 40 years, virtually all people with DS have sufficient neuropathology for a postmortem diagnosis of Alzheimer disease (AD). Trisomy 21 in DS leads to an overexpression of many proteins, of which at least two are involved in oxidative stress and AD: superoxide dismutase 1 (SOD1) and amyloid precursor protein (APP). In this study, we tested the hypothesis that DS brains with neuropathological hallmarks of AD have more oxidative and nitrosative stress than those with DS but without significant AD pathology, as compared with similarly aged-matched non-DS controls. The frontal cortex was examined in 70 autopsy cases (n=29 control and n=41 DS). By ELISA, we quantified soluble and insoluble Aβ40 and Aβ42, as well as oligomers. Oxidative and nitrosative stress levels (protein carbonyls, 4-hydroxy-2-trans-nonenal (HNE)-bound proteins, and 3-nitrotyrosine) were measured by slot-blot. We found that soluble and insoluble amyloid beta peptide (Aβ) and oligomers increase as a function of age in DS frontal cortex. Of the oxidative stress markers, HNE-bound proteins were increased overall in DS. Protein carbonyls were correlated with Aβ40 levels. These results suggest that oxidative damage, but not nitrosative stress, may contribute to the onset and progression of AD pathogenesis in DS. Conceivably, treatment with antioxidants may provide a point of intervention to slow pathological alterations in DS.

Key findings

In this study, we tested the hypothesis that DS brains with neuropathological hallmarks of AD have more oxidative and nitrosative stress than those with DS but without significant AD pathology, as compared with similarly aged-matched non-DS controls.
We found that soluble and insoluble amyloid beta peptide (Aβ) and oligomers increase as a function of age in DS frontal cortex.
Of the oxidative stress markers, HNE-bound proteins were increased overall in DS.
These results suggest that oxidative damage, but not nitrosative stress, may contribute to the onset and progression of AD pathogenesis in DS.

Why it matters

In 70 autopsy cases, this study found that soluble and insoluble amyloid beta and oligomers increase with age in the frontal cortex of people with Down syndrome, and that one marker of oxidative damage, HNE-bound proteins, was increased overall. It suggests oxidative damage, but not nitrosative stress, may contribute to Alzheimer's disease in Down syndrome, but it is an observational tissue study and tests no treatment.

Study details

Participants29
Evidence strengthLow

How this study scored 47/100

Published in a peer-reviewed journal. Scored zero for study design, effect reported 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 45 of the 96 points we could judge it on, which is 47 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	1 / 4	29 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 123 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	7.7 citations a year over 16 year(s) since 2012
Impact for its field and year	4 / 6	Cited 8.9× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 26 other studies in this library
Still being cited	1 / 4	Cited 11 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Elizabeth Head: h-index 98 (OpenAlex, whole career)
Institution's track record	1 / 3	University of California, Irvine: institution h-index 1,195 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 22009041)
Free to read	0 / 2	Behind a paywall — scores zero
Points	45 / 96	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 45 of the 96 points we could judge it on is 47 out of 100.
Total	47 / 100	—

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

Read the original

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

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APA 7th

Cenini, G., Dowling, A. L., Beckett, T. L., Barone, E., Mancuso, C., Murphy, M. P., et al. (2012). Association between frontal cortex oxidative damage and beta-amyloid as a function of age in Down syndrome. Biochimica et biophysica acta. https://doi.org/10.1016/j.bbadis.2011.10.001

Vancouver

Cenini G, Dowling AL, Beckett TL, Barone E, Mancuso C, Murphy MP, et al. Association between frontal cortex oxidative damage and beta-amyloid as a function of age in Down syndrome. Biochimica et biophysica acta. 2012. doi:10.1016/j.bbadis.2011.10.001. PMID: 22009041.

BibTeX

@article{cenini2012-22009041,
  author  = {Cenini, G. and Dowling, A. L. and Beckett, T. L. and Barone, E. and Mancuso, C. and Murphy, M. P. and Levine, H. and Lott, I. T. and others},
  title   = {{Association between frontal cortex oxidative damage and beta-amyloid as a function of age in Down syndrome}},
  journal = {Biochimica et biophysica acta},
  year    = {2012},
  doi     = {10.1016/j.bbadis.2011.10.001},
  pmid    = {22009041},
  url     = {https://doi.org/10.1016/j.bbadis.2011.10.001}
}

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