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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.

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Prevention and risk

Topic: Amyloid, tau and blood-test diagnosis

We propose that increased formation of oxygen-derived free radicals, such as the superoxide and hydroxyl species, may be responsible for progressive neural degeneration in dementia of the Alzheimer type (DAT). Several processes increase free radical formation and some of them (e.g., brain trauma, aging) are risk factors for DAT. There is some evidence for increased free radical formation in Down's syndrome which is associated with development of DAT pathology. Free radicals alone may induce cell death by damaging lipids or proteins while reactions between free radicals and neurotransmitters may lead to formation of endogenous neurotoxin(s). Recently, we have demonstrated that partial oxidation of serotonin by exposure to hydroxyl radicals results in formation of a novel neurotoxin, tryptamine-4,5-dione. Elucidation of the role of free radicals in DAT could open new avenues to prevention and treatment of this disease.

Key findings

Why it matters

This paper proposes a hypothesis that increased formation of oxygen-derived free radicals may cause progressive nerve degeneration in Alzheimer's disease. It is a hypothesis based on laboratory observations, not a tested treatment, and the authors say clarifying the role of free radicals could open new avenues for prevention and treatment.

Study details

How this study scored 41/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 2 of 5; Impact for its field and year 3 of 6; Cited by studies here 2 of 6; Still being cited 0 of 4; Senior author's track record 3 of 4; Institution's track record 1 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 41 of 100.41 of 100 points earned59 not earned

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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neurobiology of aging)
Journal's citation record 3 / 4 Neurobiology of Aging: journal h-index 263 (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 1990 — 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 190 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 5.0 citations a year over 38 year(s) since 1990
Impact for its field and year 3 / 6 Cited 7.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 2 / 6 Cited by 3 other studies in this library
Still being cited 0 / 4 Cited 2 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Peter B. Crino: h-index 69 (OpenAlex, whole career)
Institution's track record 1 / 3 Boston University: institution h-index 1,456 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 2146522)
Free to read 0 / 2 Behind a paywall — scores zero
Total 41 / 100 —

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

Read the original

May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), so the publisher may charge for it. The PubMed abstract is free.

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

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.

APA 7th

Volicer, L., & Crino, P. B. (1990). Involvement of free radicals in dementia of the Alzheimer type: a hypothesis. Neurobiology of aging. https://doi.org/10.1016/0197-4580(90)90119-k

Vancouver

Volicer L, Crino PB. Involvement of free radicals in dementia of the Alzheimer type: a hypothesis. Neurobiology of aging. 1990. doi:10.1016/0197-4580(90)90119-k. PMID: 2146522.

BibTeX

@article{volicer1990-2146522,
  author  = {Volicer, L. and Crino, P. B.},
  title   = {{Involvement of free radicals in dementia of the Alzheimer type: a hypothesis}},
  journal = {Neurobiology of aging},
  year    = {1990},
  doi     = {10.1016/0197-4580(90)90119-k},
  pmid    = {2146522},
  url     = {https://doi.org/10.1016/0197-4580(90)90119-k}
}

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