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43/100

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. Here, we show that in Drosophila, the targeted expression of the key genes of AD, APP, the beta-site APP-cleaving enzyme BACE, and the presenilins led to the generation of beta-amyloid plaques and age-dependent neurodegeneration as well as to semilethality, a shortened life span, and defects in wing vein development. Genetic manipulations or pharmacological treatments with secretase inhibitors influenced the activity of the APP-processing proteases and modulated the severity of the phenotypes.

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

APA 7th

Greeve, I., Kretzschmar, D., Tschäpe, J. A., Beyn, A., Brellinger, C., Schweizer, M., et al. (2004). Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.0283-04.2004

Vancouver

Greeve I, Kretzschmar D, Tschäpe JA, Beyn A, Brellinger C, Schweizer M, et al. Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2004. doi:10.1523/jneurosci.0283-04.2004. PMID: 15102905.

BibTeX

@article{greeve2004-15102905,
  author  = {Greeve, I. and Kretzschmar, D. and Tschäpe, J. A. and Beyn, A. and Brellinger, C. and Schweizer, M. and Nitsch, R. M. and Reifegerste, R.},
  title   = {{Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila}},
  journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year    = {2004},
  doi     = {10.1523/jneurosci.0283-04.2004},
  pmid    = {15102905},
  url     = {https://doi.org/10.1523/jneurosci.0283-04.2004}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

Key findings

Here, we show that in Drosophila, the targeted expression of the key genes of AD, APP, the beta-site APP-cleaving enzyme BACE, and the presenilins led to the generation of beta-amyloid plaques and age-dependent neurodegeneration as well as to semilethality, a shortened life span, and defects in wing vein development.
Genetic manipulations or pharmacological treatments with secretase inhibitors influenced the activity of the APP-processing proteases and modulated the severity of the phenotypes.
This invertebrate model of amyloid plaque pathology demonstrates Abeta-induced neurodegeneration as a basic biological principle and may allow additional genetic analyses of the underlying molecular pathways.

Why it matters

In fruit flies engineered to express APP, BACE and presenilins, beta-amyloid plaques and age-dependent neurodegeneration appeared, and secretase inhibitors changed the severity of these effects. This is an animal model, so it does not show that such inhibitors help people with Alzheimer's disease.

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Study details

Evidence strengthLow

How this study scored 43/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (The Journal of neuroscience : the official journal of the Society for Neuroscience)
Journal's citation record	4 / 4	Journal of Neuroscience: journal h-index 651 (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	2004 — 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	Laboratory or animal study (title names “transgenic”) — scores zero
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 288 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	12.0 citations a year over 24 year(s) since 2004
Impact for its field and year	3 / 6	Cited 7.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	1 / 6	Cited by 1 other studies in this library
Still being cited	2 / 4	Cited 29 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Rita Reifegerste: h-index 11 (OpenAlex, whole career)
Institution's track record	1 / 3	University of Zurich: institution h-index 1,220 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 5 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 15102905)
Free to read	0 / 2	Behind a paywall — scores zero
Total	43 / 100	—

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