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46/100

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Down syndrome and Alzheimer's

Topic: Brain proteins, microglia and lab models

Plain-language summary

Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes. Indeed, currently life expectancy and quality of life for DS patients have improved, although with increasing age pathological dysfunctions are exacerbated and intellectual disability may lead to the development of Alzheimer's type dementia (AD). The neuropathology of DS is complex and includes the development of AD by middle age, altered free radical metabolism, and impaired mitochondrial function, both of which contribute to neuronal degeneration. Understanding the molecular basis that drives the development of AD is an intense field of research. Our laboratories are interested in understanding the role of oxidative stress as link between DS and AD. This review examines the current literature that showed oxidative damage in DS by identifying putative molecular pathways that play a central role in the neurodegenerative processes. In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients.

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

APA 7th

Perluigi, M., & Butterfield, D. A. (2012). Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia. Current gerontology and geriatrics research. https://doi.org/10.1155/2012/724904

Vancouver

Perluigi M, Butterfield DA. Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia. Current gerontology and geriatrics research. 2012. doi:10.1155/2012/724904. PMID: 22203843.

BibTeX

@article{perluigi2012-22203843,
  author  = {Perluigi, M. and Butterfield, D. A.},
  title   = {{Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia}},
  journal = {Current gerontology and geriatrics research},
  year    = {2012},
  doi     = {10.1155/2012/724904},
  pmid    = {22203843},
  url     = {https://doi.org/10.1155/2012/724904}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients.

Why it matters

This review examines evidence that oxidative stress and impaired mitochondrial function may link Down syndrome to the later development of Alzheimer-like dementia. It proposes molecular pathways for further research and reports no treatment, cure or prevention.

Study details

Evidence strengthLow

How this study scored 46/100

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 (Current gerontology and geriatrics research)
Journal's citation record	0 / 4	Current Gerontology and Geriatrics Research: journal h-index 52 (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	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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 185 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	11.6 citations a year over 16 year(s) since 2012
Impact for its field and year	4 / 6	Cited 12.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 22 other studies in this library
Still being cited	2 / 4	Cited 28 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	Sapienza University of Rome: institution h-index 1,145 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 22203843)
Free to read	2 / 2	Free to read
Total	46 / 100	—

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