The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity
Open accessAbstract
The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. Microglial defects in phagocytosis of toxic aggregates or apoptotic membranes were proposed to be at the origin of the pathological processes in the presence of Trem2 inactivating mutations. Here, we show that TREM2 is essential for microglia-mediated synaptic refinement during the early stages of brain development. The absence of Trem2 resulted in impaired synapse elimination, accompanied by enhanced excitatory neurotransmission and reduced long-range functional connectivity. Trem2 -/- mice displayed repetitive behavior and altered sociability. TREM2 protein levels were also negatively correlated with the severity of symptoms in humans affected by autism. These data unveil the role of TREM2 in neuronal circuit sculpting and provide the evidence for the receptor's involvement in neurodevelopmental diseases.
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From Sex chromosomes and sex hormones differently shape microglial properties during normal physiological conditions in the adult mouse hippocampus (2025) · cites this paper as [25]
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- Authors
- Filipello, F., Morini, R., Corradini, I., Zerbi, V., Canzi, A., Michalski, B., Erreni, M., Markicevic, M., Starvaggi-Cucuzza, C., Otero, K., Piccio, L., Cignarella, F., Perrucci, F., Tamborini, M., Genua, M., Rajendran, L., Menna, E., Vetrano, S., Fahnestock, M., Paolicelli, R. C., & Matteoli, M.
- Affiliations
- Humanitas University (IT)
- IRCCS Humanitas Research Hospital (IT)
- ETH Zurich (CH)
- McMaster University (CA)
- Biogen (United States) (US)
- Washington University in St. Louis (US)
- University of Zurich (CH)
- Corresponding author
- Matteoli, Michela
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2018-05
- Volume
- 48
- Issue
- 5
- Pages
- 979-991.e8
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2801885674
- Cited by
- 695
- References
- 31
- Citations by year
- 2026: 81 · 2025: 89 · 2024: 100 · 2023: 103 · 2022: 90 · 2021: 88 · 2020: 74 · 2019: 50 · 2018: 16
- FWCI
- 26.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Ministero della Salute (GR-2011–02347377)
- Cariplo (2015–0594)
- AMANDA (CUP_B42F16000440005)
- Fondazione Vodafone
- Ontario Mental Health Foundation
- Fondazione Umberto Veronesi
- Fondazione Giancarla Vollaro
- ETH (SEED-42 16-1, ETH-38 16-2)
- SNSF AMBIZIONE (PZ00P3_173984 / 1)
- Synapsis Foundation - Alzheimer Research Switzerland ARS
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- TREM2, microglia, synaptic pruning, brain connectivity, excitatory neurotransmission, long-range functional connectivity, repetitive behavior, sociability, autism spectrum disorder, neurodevelopmental disorders, Alzheimer's disease, Nasu-Hakola disease, TREM2 knockout mice
- MeSH terms
- Animals, Autistic Disorder, Brain, Cells, Cultured, Humans, Membrane Glycoproteins, Mice, Inbred C57BL, Synaptic Transmission, Neurons, Receptors, Immunologic, Synapses, Microglia, Mice, Knockout
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