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48/100

✓ Peer-reviewed alzhub usefulness score 48 out of 100. TREM2 and immune genetics

Topic: Brain proteins, microglia and lab models

Plain-language summary

Mutations in triggering receptor expressed on myeloid cells 2 (TREM2), which has been proposed to regulate the inflammatory responses and the clearance of apoptotic neurons and/or amyloid-β, are genetically linked to increased risk for late-onset Alzheimer's disease (AD). Interestingly, a missense variant in TREM-like transcript 2 (TREML2), a structurally similar protein encoded by the same gene cluster with TREM2 on chromosome 6, has been shown to protect against AD. However, the molecular mechanisms by which TREM2 and TREML2 regulate the pathogenesis of AD, and their functional relationship, if any, remain unclear.

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

APA 7th

Zheng, H., Liu, C. C., Atagi, Y., Chen, X. F., Jia, L., Yang, L., et al. (2016). Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2016.03.004

Vancouver

Zheng H, Liu CC, Atagi Y, Chen XF, Jia L, Yang L, et al. Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation. Neurobiology of aging. 2016. doi:10.1016/j.neurobiolaging.2016.03.004. PMID: 27143430.

BibTeX

@article{zheng2016-27143430,
  author  = {Zheng, H. and Liu, C. C. and Atagi, Y. and Chen, X. F. and Jia, L. and Yang, L. and He, W. and Zhang, X. and others},
  title   = {{Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation}},
  journal = {Neurobiology of aging},
  year    = {2016},
  doi     = {10.1016/j.neurobiolaging.2016.03.004},
  pmid    = {27143430},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2016.03.004}
}

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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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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

Interestingly, a missense variant in TREM-like transcript 2 (TREML2), a structurally similar protein encoded by the same gene cluster with TREM2 on chromosome 6, has been shown to protect against AD.
However, the molecular mechanisms by which TREM2 and TREML2 regulate the pathogenesis of AD, and their functional relationship, if any, remain unclear.
Here, we show that lipopolysaccharide (LPS) stimulation significantly suppressed TREM2 but increased TREML2 expression in mouse brain.
Consistent with this in vivo result, LPS or oligomeric amyloid-β treatment down regulated TREM2 but up-regulated TREML2 expression in primary microglia.

Why it matters

TREM2 is a known Alzheimer's risk gene, and a variant in its neighbour TREML2 has been reported to protect against the disease. In mice, this study found that an inflammatory trigger (LPS) "significantly suppressed TREM2 but increased TREML2 expression" in the brain, and that LPS or amyloid-β oligomers did the same in microglia grown in a dish. These are expression changes in mouse models, not human results, and they do not point to any treatment.

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Study details

Evidence strengthLow

How this study scored 48/100

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 (Neurobiology of aging)
Journal's citation record	3 / 4	Neurobiology of Aging: journal h-index 263 (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	2016 — 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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 110 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	9.2 citations a year over 12 year(s) since 2016
Impact for its field and year	3 / 6	Cited 4.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 26 other studies in this library
Still being cited	2 / 4	Cited 24 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Guojun Bu: h-index 120 (OpenAlex, whole career)
Institution's track record	2 / 3	Mayo Clinic: institution h-index 1,606 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 4 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 27143430)
Free to read	0 / 2	Behind a paywall — scores zero
Total	48 / 100	—

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