This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

36/100

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

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Genetic and lifestyle-related risk factors for Alzheimer disease (AD) are associated with an increase in oxidative stress, suggesting that oxidative stress is involved at an early stage of the pathologic cascade. Moreover, oxidative stress is mechanistically and chronologically associated with other key features of AD, namely, metabolic, mitochondrial, metal, and cell-cycle abnormalities. Contrary to the commonly held notion that pathologic hallmarks of AD signify etiology, several lines of evidence now indicate that aggregation of amyloid-beta and tau is a compensatory response to underlying oxidative stress. Therefore, removal of proteinaceous accumulations may treat the epiphenomenon rather than the disease and may actually enhance oxidative damage. Although some antioxidants have been shown to reduce the incidence of AD, the magnitude of the effect may be modified by individual factors such as genetic predisposition (e.g. apolipoprotein E genotype) and habitual behaviors. Because caloric restriction, exercise, and intellectual activity have been experimentally shown to promote neuronal survival through enhancement of endogenous antioxidant defenses, a combination of dietary regimen of low total calorie and rich antioxidant nutrients and maintaining physical and intellectual activities may ultimately prove to be one of the most efficacious strategies for AD prevention.

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

APA 7th

Nunomura, A., Castellani, R. J., Zhu, X., Moreira, P. I., Perry, G., & Smith, M. A. (2006). Involvement of oxidative stress in Alzheimer disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/01.jnen.0000228136.58062.bf

Vancouver

Nunomura A, Castellani RJ, Zhu X, Moreira PI, Perry G, Smith MA. Involvement of oxidative stress in Alzheimer disease. Journal of neuropathology and experimental neurology. 2006. doi:10.1097/01.jnen.0000228136.58062.bf. PMID: 16825950.

BibTeX

@article{nunomura2006-16825950,
  author  = {Nunomura, A. and Castellani, R. J. and Zhu, X. and Moreira, P. I. and Perry, G. and Smith, M. A.},
  title   = {{Involvement of oxidative stress in Alzheimer disease}},
  journal = {Journal of neuropathology and experimental neurology},
  year    = {2006},
  doi     = {10.1097/01.jnen.0000228136.58062.bf},
  pmid    = {16825950},
  url     = {https://doi.org/10.1097/01.jnen.0000228136.58062.bf}
}

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.

How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
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.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Genetic and lifestyle-related risk factors for Alzheimer disease (AD) are associated with an increase in oxidative stress, suggesting that oxidative stress is involved at an early stage of the pathologic cascade.
Moreover, oxidative stress is mechanistically and chronologically associated with other key features of AD, namely, metabolic, mitochondrial, metal, and cell-cycle abnormalities.
Contrary to the commonly held notion that pathologic hallmarks of AD signify etiology, several lines of evidence now indicate that aggregation of amyloid-beta and tau is a compensatory response to underlying oxidative stress.

New to this subject? Start with our plain-English guide: Genetics →

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 (Journal of neuropathology and experimental neurology)
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 16825950)
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 →

Read the original

Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.

Studies in the library that share something with this one. The line above each title says what.

Related studies in Genetics from nearby years

Also tagged “involvement”

3 studies in the library carry the topic tag “involvement”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 3 tagged studies.

Studies sharing this one's topic tags

Similar studies

More on Genetics

See all studies in Genetics →