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40/100

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from beta-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E and Ginkgo biloba extract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, beta-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.

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

APA 7th

Grundman, M., & Delaney, P. (2002). Antioxidant strategies for Alzheimer's disease. The Proceedings of the Nutrition Society. https://doi.org/10.1079/pns2002146

Vancouver

Grundman M, Delaney P. Antioxidant strategies for Alzheimer's disease. The Proceedings of the Nutrition Society. 2002. doi:10.1079/pns2002146. PMID: 12133201.

BibTeX

@article{grundman2002-12133201,
  author  = {Grundman, M. and Delaney, P.},
  title   = {{Antioxidant strategies for Alzheimer's disease}},
  journal = {The Proceedings of the Nutrition Society},
  year    = {2002},
  doi     = {10.1079/pns2002146},
  pmid    = {12133201},
  url     = {https://doi.org/10.1079/pns2002146}
}

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Key findings

In AD clinical trials molecules with antioxidant properties such as vitamin E and Ginkgo biloba extract have shown modest benefit.
A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment.
Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone).
Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, beta-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry.
Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.

Why it matters

This review notes that vitamin E and Ginkgo biloba extract have shown only modest benefit in Alzheimer's clinical trials, and a trial of vitamin E in mild cognitive impairment was ongoing. Combinations of antioxidants might have greater potential, but this is not established and no cure is claimed.

Study details

Evidence strengthLow

How this study scored 40/100

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. We have no data on senior author's track record, so that was left out: it earned 38 of the 96 points we could judge it on, which is 40 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (The Proceedings of the Nutrition Society)
Journal's citation record	2 / 4	Proceedings of The Nutrition Society: journal h-index 193 (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	2002 — 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 194 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	7.5 citations a year over 26 year(s) since 2002
Impact for its field and year	3 / 6	Cited 6.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 5 other studies in this library
Still being cited	1 / 4	Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	2 / 3	University of California San Diego: institution h-index 1,852 (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 12133201)
Free to read	0 / 2	Behind a paywall — scores zero
Points	38 / 96	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 38 of the 96 points we could judge it on is 40 out of 100.
Total	40 / 100	—

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

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