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Cited by 427Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsInflammation biomarkers and pathways

TREM2 in Neurodegenerative Diseases

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Jay, Taylor R., von Saucken, Victoria E., Landreth, Gary E.·2017·Molecular Neurodegeneration
DOI 10.1186/s13024-017-0197-5PMC PMC5541421
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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.

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  • TREM2 activation supports microglia's migration toward amyloid plaques, preventing amyloid spread.

    “Ordinarily, TREM2 activation is considered as a beneficial response in that it supports microglia’s migration toward amyloid plaques, preventing amyloid spread221–224”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [222]

    The sections on TREM2 function and amyloid pathology report that TREM2 is required for myeloid-cell accumulation around plaques and that plaque-associated cells have been proposed to limit plaque growth by forming a barrier. The claim presents prevention of amyloid spread as an established effect, whereas the paper frames the barrier mechanism as a proposal, particularly for later disease progression. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • TREM2 plays a key and enigmatic role in the progression of AD, acting to drive microglial phagocytosis, survival, lipid homeostasis, and metabolism.

    “TREM2 plays a key and enigmatic role in the progression of AD, acting to drive microglial phagocytosis, survival, lipid homeostasis, and metabolism.”

    From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [37]

    The sections on phagocytic function and myeloid-cell survival support TREM2’s roles in Aβ uptake and microglial survival, while the AD pathology section describes a complex, stage-dependent role in disease progression (page numbers unavailable). The “Other functions of TREM2” section links deficiency to altered lipid metabolism in a mouse demyelination model but treats a broader lipid-related role as a possibility; it does not establish that TREM2 drives microglial lipid homeostasis or metabolism in AD. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • TREM2 loss-of-function impairs microglial protective functions and worsens neuronal dystrophy.

    “TREM2 loss‐of‐function impairs microglial protective functions and worsens neuronal dystrophy. 9 , 37 , 38 , 41 , 42 , 61”

    From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [37]

    The section “TREM2 modulates neuritic dystrophy in AD” reports increased dystrophy around plaques in TREM2-deficient mice and human R47H carriers with AD. It also suggests that TREM2 enables microglial clustering that may form a protective barrier, but cautions that not all evidence supports a protective role. The claim presents that proposed protective function as established and does not limit the dystrophy finding to the AD plaque setting. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • In AD, amyloid pathology induces the expression of TREM2 in microglia.

    “In AD, amyloid pathology induces the expression of TREM2 in microglia. 36 , 37 , 38 , 39 , 40 , 41 , 60”

    From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [37]

    The “TREM2 expression” section reports plaque-associated upregulation and says the findings suggest amyloid can increase TREM2 expression in myeloid cells. It also says results in cultured microglia are inconsistent and that studies conflict over whether the TREM2-expressing cells are resident microglia or other myeloid cells. The claim states the causal effect specifically in microglia more definitively than the source does; page numbers were not supplied. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Jay, T. R., von Saucken, V. E., & Landreth, G. E.
Affiliations
  • Case Western Reserve University (US)
  • Indiana University School of Medicine (US)
Corresponding author
Landreth, Gary E.
ORCID
Venue
Molecular Neurodegeneration
Publisher
Springer Science and Business Media LLC
Published
2017-08-02
Volume
12
Issue
1
Pages
56-56
ISSN
1750-1326 (ISSN-L)
DOI
10.1186/s13024-017-0197-5
PMC
PMC5541421
OpenAlex
W2741386819
Cited by
427
References
63
Citations by year
2026: 24 · 2025: 62 · 2024: 53 · 2023: 59 · 2022: 47 · 2021: 46 · 2020: 47 · 2019: 44 · 2018: 41 · 2017: 4
FWCI
3.59
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Neurodegeneration (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • IUScholarWorks (Indiana University) (submittedVersion, cc-by)
  • PMC
Funders
  • National Institute on Aging (RF1 AG051495, R01 AG050597, F31 AG048704)
  • Alzheimer's Association (BFG-15-364590)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
TREM2, neurodegenerative diseases, Alzheimer's disease, genetic risk factors, TREM2 signaling, neuroinflammation, microglia, biomarkers, therapeutics
MeSH terms
Animals, Disease Models, Animal, Humans, Membrane Glycoproteins, Receptors, Immunologic, Biomarkers, Microglia, Disease Progression, Neurodegenerative Diseases

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