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50/100

✓ Peer-reviewed alzhub usefulness score 50 out of 100. TREM2 and immune genetics

Topic: Brain proteins, microglia and lab models

Plain-language summary

Variants of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased incidence of Alzheimer's disease, as well as other neurodegenerative disorders. Using a newly developed, highly sensitive reporter cell model, consisting of Jurkat T cells stably overexpressing a reporter gene and a gene encoding TREM2DAP12 fusion protein, we show here that TREM2-dependent signal transduction in response to apoptotic Neuro2a cells is mediated by aminophospholipid ligands, phosphatidylserine and phosphatidylethanolamine, which are not exposed on the intact cell surface, but become exposed upon apoptosis. We also show that signal-transducing TREM2 ligands different from aminophospholipids, which appear to be derived from neurons, might be present in membrane fractions of mouse cerebral cortex.

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APA 7th

Shirotani, K., Hori, Y., Yoshizaki, R., Higuchi, E., Colonna, M., Saito, T., et al. (2019). Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells. Scientific reports. https://doi.org/10.1038/s41598-019-43535-6

Vancouver

Shirotani K, Hori Y, Yoshizaki R, Higuchi E, Colonna M, Saito T, et al. Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells. Scientific reports. 2019. doi:10.1038/s41598-019-43535-6. PMID: 31101881.

BibTeX

@article{shirotani2019-31101881,
  author  = {Shirotani, K. and Hori, Y. and Yoshizaki, R. and Higuchi, E. and Colonna, M. and Saito, T. and Hashimoto, S. and others},
  title   = {{Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells}},
  journal = {Scientific reports},
  year    = {2019},
  doi     = {10.1038/s41598-019-43535-6},
  pmid    = {31101881},
  url     = {https://doi.org/10.1038/s41598-019-43535-6}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
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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

Using a newly developed, highly sensitive reporter cell model, consisting of Jurkat T cells stably overexpressing a reporter gene and a gene encoding TREM2DAP12 fusion protein, we show here that TREM2-dependent signal transduction in response to apoptotic Neuro2a cells is mediated by aminophospholipid ligands, phosphatidylserine and phosphatidylethanolamine, which are not exposed on the intact cell surface, but become exposed upon apoptosis.
We also show that signal-transducing TREM2 ligands different from aminophospholipids, which appear to be derived from neurons, might be present in membrane fractions of mouse cerebral cortex.
These results may suggest that TREM2 regulates microglial function by transducing intracellular signals from aminophospholipids on apoptotic cells, as well as unidentified ligands in the membranes of the cerebral cortex.

Why it matters

TREM2 gene variants are linked to a higher risk of Alzheimer's disease. Using a newly built lab reporter cell, this study found that TREM2 is switched on by two fats, phosphatidylserine and phosphatidylethanolamine, which are hidden inside healthy cells and become exposed only when a cell dies. It also found hints of other, still-unidentified TREM2 triggers in mouse brain membranes. This is cell and mouse-tissue lab work: the authors say it "may suggest" how TREM2 guides the brain's immune cells, and it does not test any treatment.

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Study details

Evidence strengthLow

How this study scored 50/100

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 (Scientific reports)
Journal's citation record	3 / 4	Scientific Reports: journal h-index 463 (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	2 / 5	2019 — within 10 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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 117 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	13.0 citations a year over 9 year(s) since 2019
Impact for its field and year	3 / 6	Cited 5.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 14 other studies in this library
Still being cited	2 / 4	Cited 43 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Nobuhisa Iwata: h-index 55 (OpenAlex, whole career)
Institution's track record	2 / 3	Washington University in St. Louis: institution h-index 1,962 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 4 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 31101881)
Free to read	2 / 2	Free to read
Total	50 / 100	—

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