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.

44/100

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease. Small molecule γ-secretase modulators (GSMs) have emerged as potential disease-modifying treatments for Alzheimer disease because they reduce the formation of Aβ42 while not blocking the processing of γ-secretase substrates.

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

APA 7th

Pozdnyakov, N., Murrey, H. E., Crump, C. J., Pettersson, M., Ballard, T. E., Am Ende, C. W., et al. (2013). γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m112.398602

Vancouver

Pozdnyakov N, Murrey HE, Crump CJ, Pettersson M, Ballard TE, Am Ende CW, et al. γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin. The Journal of biological chemistry. 2013. doi:10.1074/jbc.m112.398602. PMID: 23396974.

BibTeX

@article{pozdnyakov2013-23396974,
  author  = {Pozdnyakov, N. and Murrey, H. E. and Crump, C. J. and Pettersson, M. and Ballard, T. E. and Am Ende, C. W. and Ahn, K. and Li, Y. M. and others},
  title   = {{γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin}},
  journal = {The Journal of biological chemistry},
  year    = {2013},
  doi     = {10.1074/jbc.m112.398602},
  pmid    = {23396974},
  url     = {https://doi.org/10.1074/jbc.m112.398602}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Aβ42) that have been implicated in the pathogenesis of Alzheimer disease.
Small molecule γ-secretase modulators (GSMs) have emerged as potential disease-modifying treatments for Alzheimer disease because they reduce the formation of Aβ42 while not blocking the processing of γ-secretase substrates.
We developed clickable GSM photoaffinity probes with the goal of identifying the target of various classes of GSMs and to better understand their mechanism of action.
Here, we demonstrate that the photoaffinity probe E2012-BPyne specifically labels the N-terminal fragment of presenilin-1 (PS1-NTF) in cell membranes as well as in live cells and primary neuronal cultures.

Why it matters

This laboratory study used photoaffinity probes to show that different classes of gamma-secretase modulators bind to distinct allosteric sites on presenilin. It clarifies how these compounds work but does not show that they treat, cure, or prevent Alzheimer's disease in people.

New to this subject? Start with our plain-English guide: Genetics →

Study details

Evidence strengthLow

How this study scored 44/100

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.

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	2013 — within 20 year(s) of the newest study here
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 107 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	7.1 citations a year over 15 year(s) since 2013
Impact for its field and year	4 / 6	Cited 9.4× 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	1 / 4	Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Douglas S. Johnson: h-index 40 (OpenAlex, whole career)
Institution's track record	2 / 3	Memorial Sloan Kettering Cancer Center: institution h-index 1,931 (OpenAlex)
Multi-centre collaboration	2 / 3	OpenAlex lists 4 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 23396974)
Free to read	0 / 2	Behind a paywall — scores zero
Total	44 / 100	—

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

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Studies this one cites

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

Later studies that cite this one

1 study in the alzhub library lists this one in its references.

Related studies in Risk genes beyond APOE

Also tagged “tdp-43”

1,150 studies in the library carry the topic tag “tdp-43”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 1,150 tagged studies.

Similar studies

More on Risk genes beyond APOE

See all studies in Risk genes beyond APOE →