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36/100

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer's disease (AD), the leading cause of dementia, involves regionalized neuronal death, synaptic loss, and an accumulation of intraneuronal, neurofibrillary tangles and extracellular senile plaques. Although the initiating causes leading to AD are unknown, a number of previous studies reported the role of oxidative stress in AD brain. Postmortem analysis of AD brain showed elevated markers of oxidative stress including protein nitrotyrosine, carbonyls in proteins, lipid oxidation products, and oxidized DNA bases. In this review, we focus our attention on the role of protein oxidation and lipid peroxidation in the pathogenesis of AD. Particular attention is given to the current knowledge about the redox proteomics identification of oxidatively modified proteins in AD brain.

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APA 7th

Sultana, R., Perluigi, M., & Butterfield, D. A. (2006). Protein oxidation and lipid peroxidation in brain of subjects with Alzheimer's disease: insights into mechanism of neurodegeneration from redox proteomics. Antioxidants & redox signaling. https://doi.org/10.1089/ars.2006.8.2021

Vancouver

Sultana R, Perluigi M, Butterfield DA. Protein oxidation and lipid peroxidation in brain of subjects with Alzheimer's disease: insights into mechanism of neurodegeneration from redox proteomics. Antioxidants & redox signaling. 2006. doi:10.1089/ars.2006.8.2021. PMID: 17034347.

BibTeX

@article{sultana2006-17034347,
  author  = {Sultana, R. and Perluigi, M. and Butterfield, D. A.},
  title   = {{Protein oxidation and lipid peroxidation in brain of subjects with Alzheimer's disease: insights into mechanism of neurodegeneration from redox proteomics}},
  journal = {Antioxidants \& redox signaling},
  year    = {2006},
  doi     = {10.1089/ars.2006.8.2021},
  pmid    = {17034347},
  url     = {https://doi.org/10.1089/ars.2006.8.2021}
}

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How to read this study

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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

Alzheimer's disease (AD), the leading cause of dementia, involves regionalized neuronal death, synaptic loss, and an accumulation of intraneuronal, neurofibrillary tangles and extracellular senile plaques.
Although the initiating causes leading to AD are unknown, a number of previous studies reported the role of oxidative stress in AD brain.
Postmortem analysis of AD brain showed elevated markers of oxidative stress including protein nitrotyrosine, carbonyls in proteins, lipid oxidation products, and oxidized DNA bases.
In this review, we focus our attention on the role of protein oxidation and lipid peroxidation in the pathogenesis of AD.
Particular attention is given to the current knowledge about the redox proteomics identification of oxidatively modified proteins in AD brain.

Study details

Evidence strengthLow

How this study scored 36/100

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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Antioxidants & redox signaling)
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	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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	— / 7	No citation count (not found in OpenAlex) — left out of this score
Citations per year	— / 5	No citation count or no year — left out of this score
Impact for its field and year	— / 6	No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here	— / 6	Not yet checked against this library's citation graph — left out of this score
Still being cited	— / 4	No yearly citation counts — left out of this score
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 17034347)
Free to read	0 / 2	Behind a paywall — scores zero
Points	21 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100.
Total	36 / 100	—

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

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