Evidence map›Paper›PMID 28768545›Full record

ReviewMolecular neurodegeneration2017

TREM2 in Neurodegenerative Diseases.

Taylor R Jay, Victoria E von Saucken, Gary E Landreth

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 277 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
277citing papers in PubMed, 2 pooled it
15.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

277 citing papers in PubMed, 2 syntheses or guidelines pooled it, 429 citations in OpenAlex.

  1. Pooled it
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  6. Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026
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217 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Taylor R JayDepartment of Neurosciences, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH, 44106, USA.
Victoria E von SauckenDepartment of Neurosciences, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH, 44106, USA.
Gary E LandrethDepartment of Neurosciences, Case Western Reserve University, School of Medicine, 10900 Euclid Avenue, Cleveland, OH, 44106, USA. glandret@iu.edu.
Case Western Reserve University · USUniversity School · US

Funding

Central and Peripheral Roles of TREM2 in Alzheimer's DiseaseRF1AG051495 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAMB, BRUCE T, LANDRETH, GARY E. · 2015 to 2015
$3.6M
Actions of Nuclear Receptors on TREM2+ myeloid cells and microglia in AD brainRF1AG050597 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LANDRETH, GARY E. · 2016 to 2016
$2.0M
The role of TREM2 in Alzheimer's disease pathogenesisF31AG048704 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI JAY, TAYLOR REAGAN · 2014 to 2017
$102k
NIA NIH HHS F31 AG048704NIA NIH HHS RF1 AG050597NIA NIH HHS RF1 AG051495
6 · The paper itself

Abstract

TREM2 variants have been identified as risk factors for Alzheimer's disease (AD) and other neurodegenerative diseases (NDDs). Because TREM2 encodes a receptor exclusively expressed on immune cells, identification of these variants conclusively demonstrates that the immune response can play an active role in the pathogenesis of NDDs. These TREM2 variants also confer the highest risk for developing Alzheimer's disease of any risk factor identified in nearly two decades, suggesting that understanding more about TREM2 function could provide key insights into NDD pathology and provide avenues for novel immune-related NDD biomarkers and therapeutics. The expression, signaling and function of TREM2 in NDDs have been extensively investigated in an effort to understand the role of immune function in disease pathogenesis and progression. We provide a comprehensive review of our current understanding of TREM2 biology, including new insights into the regulation of TREM2 expression, and TREM2 signaling and function across NDDs. While many open questions remain, the current body of literature provides clarity on several issues. While it is still often cited that TREM2 expression is decreased by pro-inflammatory stimuli, it is now clear that this is true in vitro, but inflammatory stimuli in vivo almost universally increase TREM2 expression. Likewise, while TREM2 function is classically described as promoting an anti-inflammatory phenotype, more than half of published studies demonstrate a pro-inflammatory role for TREM2, suggesting that its role in inflammation is much more complex. Finally, these components of TREM2 biology are applied to a discussion of how TREM2 impacts NDD pathologies and the latest assessment of how these findings might be applied to immune-directed clinical biomarkers and therapeutics.

Indexed as

AnimalsBiomarkersDisease Models, AnimalDisease ProgressionHumansMembrane GlycoproteinsMicrogliaNeurodegenerative DiseasesReceptors, ImmunologicBiomarkersMembrane GlycoproteinsReceptors, ImmunologicTREM2 protein, humanAlzheimer’s diseaseFrontotemporal dementiaGenetic risk factorsGeneticsInflammationMicrogliaNeurodegenerationParkinson’s diseaseTriggering receptor expressed on myeloid cells 2

Identifiers

PMID28768545
PMCPMC5541421
OpenAlexW2741386819

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.