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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

Phorbol esters, activators of protein kinase C (PKC), regulate the relative utilization of alternative processing pathways for the Alzheimer beta-amyloid precursor protein (beta-APP) in intact cells, increasing the production of nonamyloidogenic soluble beta-APP (s beta-APP) and decreasing that of neurotoxic beta-amyloid (A beta) peptide. The molecular and cellular bases of PKC-regulated beta-APP cleavage are poorly understood. Here we demonstrate in a reconstituted cell-free system that activation of endogenous PKC increases formation from the trans-Golgi network of secretory vesicles containing beta-APP and that this effect can be mimicked by purified PKC.

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

APA 7th

Xu, H., Greengard, P., & Gandy, S. (1995). Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein. The Journal of biological chemistry. https://doi.org/10.1074/jbc.270.40.23243

Vancouver

Xu H, Greengard P, Gandy S. Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein. The Journal of biological chemistry. 1995. doi:10.1074/jbc.270.40.23243. PMID: 7559474.

BibTeX

@article{xu1995-7559474,
  author  = {Xu, H. and Greengard, P. and Gandy, S.},
  title   = {{Regulated formation of Golgi secretory vesicles containing Alzheimer beta-amyloid precursor protein}},
  journal = {The Journal of biological chemistry},
  year    = {1995},
  doi     = {10.1074/jbc.270.40.23243},
  pmid    = {7559474},
  url     = {https://doi.org/10.1074/jbc.270.40.23243}
}

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Key findings

The molecular and cellular bases of PKC-regulated beta-APP cleavage are poorly understood.
Here we demonstrate in a reconstituted cell-free system that activation of endogenous PKC increases formation from the trans-Golgi network of secretory vesicles containing beta-APP and that this effect can be mimicked by purified PKC.
The results demonstrate directly that PKC is involved in regulation of secretory vesicle formation and provide a mechanism by which PKC may reduce the formation of the A beta peptide characteristic of Alzheimer disease.

Why it matters

In a cell-free system, protein kinase C activation increased formation of secretory vesicles containing beta-APP from the trans-Golgi network. This is a laboratory mechanism study and does not show that this pathway can treat, cure, or prevent Alzheimer's disease.

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Study details

Evidence strengthLow

How this study scored 45/100

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.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (The Journal of biological chemistry)
Journal's citation record	4 / 4	Journal of Biological Chemistry: journal h-index 780 (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	1995 — 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	5 / 7	Cited 169 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	5.1 citations a year over 33 year(s) since 1995
Impact for its field and year	4 / 6	Cited 8.3× 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	1 / 4	Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Sam Gandy: h-index 92 (OpenAlex, whole career)
Institution's track record	2 / 3	Cornell University: institution h-index 1,649 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 7559474)
Free to read	0 / 2	Behind a paywall — scores zero
Total	45 / 100	—

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