ArticleCNS neuroscience & therapeutics2025
Elucidating the Role of Trem2 in Lipid Metabolism and Neuroinflammation.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- Review
- Multi-functional Small Molecule for Regenerative Healing of Avascular Meniscus Tears: Modulation of Inflammation, Differentiation, and Multi-Tissue Crosstalk.Theranostics · 2026Article
- Systemic inflammation as a central player in the initiation and development of Alzheimer's disease.Immunity & ageing : I & A · 2025Review
- Microglial TREM2 and cognitive impairment: insights from Alzheimer's disease with implications for spinal cord injury and AI-assisted therapeutics.Frontiers in cellular neuroscience · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundAlzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive impairment and neuroinflammation. Astrocytes play a key role in the neuroinflammatory environment of AD, especially through lipid metabolism regulation. However, the mechanisms by which astrocytes, particularly through the triggering receptor expressed on myeloid cells 2 (Trem2) receptor, contribute to lipid dysregulation and neuroinflammation in AD remain inadequately understood.
methodsWe employed an AD mouse model and integrated single-cell RNA sequencing (scRNA-seq), transcriptomics, and high-throughput metabolomics to analyze lipid metabolism and inflammatory profiles in astrocytes. Differential gene expression was further validated with the GEO database, and in vitro and in vivo experiments were conducted to assess the impact of Trem2 modulation on astrocytic inflammation and lipid composition.
resultsOur findings demonstrate that Trem2 modulates lipid metabolism in astrocytes, affecting fatty acid and phospholipid pathways. In the AD model, Trem2 expression was suppressed, enhancing nuclear factor-κB (NF-κB) signaling and promoting the secretion of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Trem2 overexpression reduced astrocytic inflammation and altered lipid composition, attenuating neuroinflammation both in vitro and in vivo. These results underscore Trem2's regulatory role in lipid metabolism and its significant impact on neuroinflammation in AD.
conclusionsThis study identifies Trem2 as a pivotal regulator of astrocytic lipid metabolism and neuroinflammation in AD, providing potential molecular targets for early intervention and therapeutic strategies aimed at mitigating AD progression.
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