TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target
Open accessAbstract
Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer’s disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood–brain barrier, and we introduce potential pathways by which TREM2 affects the blood–brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.
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TREM2 binds to various lipid ligands to mediate lipid sensing and uptake.
“TREM2 binds to various lipid ligands, such as APOE particles (main cholesterol carriers in the brain) and myelin debris, to mediate lipid sensing and uptake (36).”
From Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model (2025) · cites this paper as [36]
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Amyloid Precursor Protein and Alzheimer’s Disease
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“TREM2 binds to various lipid ligands, such as APOE particles (main cholesterol carriers in the brain) and myelin debris, to mediate lipid sensing and uptake ( 36 ).”
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Trem2 acts as a non‐classical receptor of interleukin‐4 to promote diabetic wound healing
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- Authors
- Li, R.-Y., Qin, Q., Yang, H.-C., Wang, Y.-Y., Mi, Y.-X., Yin, Y.-S., Wang, M., Yu, C.-J., & Tang, Y.
- Affiliations
- Capital Medical University (CN)
- Corresponding author
- Tang, Yi
- Venue
- Molecular Neurodegeneration
- Published
- 2022-06-03
- Volume
- 17
- Issue
- 1
- Pages
- 40-40
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC9166437
- OpenAlex
- W4281650031
- Cited by
- 204
- References
- 205
- Citations by year
- 2026: 48 · 2025: 78 · 2024: 46 · 2023: 31 · 2022: 1
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Natural Science Foundation of Beijing Municipality (JQ19024)
- National Natural Science Foundation of China (81970996)
- Capital’s Funds for Health Improvement and Research (CFH202041033)
- National Key R&D Program of China (2017YFC1310102, 2019YFC0118200)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- TREM2, Alzheimer's disease, lipid metabolism, microglia, disease-associated microglia, cholesterol metabolism, myelin, phospholipids, obesity, hypercholesterolemia, atherosclerosis, non-alcoholic fatty liver disease, blood-brain barrier, insulin resistance, inflammation
- MeSH terms
- Alzheimer Disease, Brain, Central Nervous System, Humans, Membrane Glycoproteins, Receptors, Immunologic, Microglia, Lipid Metabolism
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