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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 37 out of 100. Down syndrome and Alzheimer's

Topic: Amyloid, tau and blood-test diagnosis

It is hypothesized that Alzheimer's disease is a human phylogenetic disease which has a common multifactorial pathogenesis in sporadic and familial cases and in Down syndrome, related to a genomic character function G(x). Increments in G(x) accompanied the increased gene expression that sustained brain growth and differentiation during hominid evolution, particularly of the regions liable to Alzheimer pathology, and further occur in Down syndrome [suggesting that genes on chromosome 21 are included in G(x)]. If genes which promoted human brain evolution contribute to the value of G(x), a better understanding of the genomic events which promoted this evolution, using molecular biological techniques, should elucidate the genetic basis of Alzheimer's disease, and vice versa.

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

APA 7th

Rapoport, S. I. (1989). Hypothesis: Alzheimer's disease is a phylogenetic disease. Medical hypotheses. https://doi.org/10.1016/0306-9877(89)90185-0

Vancouver

Rapoport SI. Hypothesis: Alzheimer's disease is a phylogenetic disease. Medical hypotheses. 1989. doi:10.1016/0306-9877(89)90185-0. PMID: 2528670.

BibTeX

@article{rapoport1989-2528670,
  author  = {Rapoport, S. I.},
  title   = {{Hypothesis: Alzheimer's disease is a phylogenetic disease}},
  journal = {Medical hypotheses},
  year    = {1989},
  doi     = {10.1016/0306-9877(89)90185-0},
  pmid    = {2528670},
  url     = {https://doi.org/10.1016/0306-9877(89)90185-0}
}

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.

Key findings

Why it matters

This paper hypothesizes that Alzheimer disease is a human phylogenetic disease with a shared cause in sporadic, familial, and Down syndrome cases. It is a hypothesis only and offers no treatment, cure, or prevention.

Study details

How this study scored 37/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 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 4 of 7; Citations per year 1 of 5; Impact for its field and year 2 of 6; Cited by studies here 0 of 6; Still being cited 1 of 4; Senior author's track record 3 of 4; Institution's track record 3 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 37 of 100.37 of 100 points earned63 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 (Medical hypotheses)
Journal's citation record 1 / 4 Medical Hypotheses: journal h-index 138 (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 1989 — 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 4 / 7 Cited 62 times (OpenAlex, 2026-10-10)
Citations per year 1 / 5 1.6 citations a year over 39 year(s) since 1989
Impact for its field and year 2 / 6 Cited 1.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 1 / 4 Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author С. И. Рапопорт: h-index 67 (OpenAlex, whole career)
Institution's track record 3 / 3 National Institutes of Health: institution h-index 2,723 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 2528670)
Free to read 0 / 2 Behind a paywall — scores zero
Total 37 / 100 —

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

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Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

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