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31/100

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Down syndrome and Alzheimer's

Topic: Brain proteins, microglia and lab models

Plain-language summary

The occurrence of +1 frameshifted proteins, such as amyloid precursor protein (APP+1) and ubiquitin-B (UBB+1) in Down syndrome (DS) has been linked to the onset of Alzheimer's disease (AD). In DS and AD patients, but also in elderly non-demented persons, these co-called +1 proteins accumulate in the neuropathological hallmarks (neurofibrillary tangles, dystrophic neurites of the neuritic plaques and neuropil threads) and may have deleterious effects on neuronal function. Frameshifts are caused by dinucleotide deletions in GAGAG motifs in messenger RNA and are now thought to be the result of unfaithful transcription of normal DNA by a novel process termed "molecular misreading". In the present review some of the critical events in molecular misreading are discussed, the emphasis being on DS.

What this study adds

Evidence grade: Low

This is a narrative review. This review describes how +1 frameshifted proteins such as APP+1 and UBB+1 accumulate in the neuropathological hallmarks of Down syndrome and Alzheimer's disease and may harm neuronal function, caused by a process the authors call molecular misreading. It is a discussion of a proposed disease mechanism and does not report or test any treatment, cure, or prevention.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

van Leeuwen, F. W., & Hol, E. M. (1999). Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration. Journal of neural transmission. Supplementum. https://doi.org/10.1007/978-3-7091-6380-1_9

Vancouver

van Leeuwen FW, Hol EM. Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration. Journal of neural transmission. Supplementum. 1999. doi:10.1007/978-3-7091-6380-1_9. PMID: 10666673.

BibTeX

@article{vanleeuwen1999-10666673,
  author  = {van Leeuwen, F. W. and Hol, E. M.},
  title   = {{Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration}},
  journal = {Journal of neural transmission. Supplementum},
  year    = {1999},
  doi     = {10.1007/978-3-7091-6380-1_9},
  pmid    = {10666673},
  url     = {https://doi.org/10.1007/978-3-7091-6380-1_9}
}

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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.

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Key findings

Frameshifts are caused by dinucleotide deletions in GAGAG motifs in messenger RNA and are now thought to be the result of unfaithful transcription of normal DNA by a novel process termed "molecular misreading".

Why it matters

This review describes how +1 frameshifted proteins such as APP+1 and UBB+1 accumulate in the neuropathological hallmarks of Down syndrome and Alzheimer's disease and may harm neuronal function, caused by a process the authors call molecular misreading. It is a discussion of a proposed disease mechanism and does not report or test any treatment, cure, or prevention.

Study details

Evidence strengthLow

How this study scored 31/100

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 and institution's track record, so those were left out: it earned 29 of the 93 points we could judge it on, which is 31 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of neural transmission. Supplementum)
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	1999 — 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	2 / 7	Cited 10 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.3 citations a year over 29 year(s) since 1999
Impact for its field and year	3 / 6	Cited 5.4× 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	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Elly M. Hol: h-index 68 (OpenAlex, whole career)
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	0 / 3	OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 10666673)
Free to read	0 / 2	Behind a paywall — scores zero
Points	29 / 93	Scored on 18 of 20 parts. We have no data for the rest, so they are left out: 29 of the 93 points we could judge it on is 31 out of 100.
Total	31 / 100	—

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

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