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The Social Dimension of Stress: Experimental Manipulations of Social Support and Social Identity in the Trier Social Stress Test
Published on: November 19, 2015
TREMendous 2 Be Social
Narghes Calcagno1, Caroline Baufeld1, Charlotte Madore1
1Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Abstract:
TREM2 is known for its role in microglial phagocytosis and in neurodegenerative diseases. In this issue of Immunity, Filipello et al. (2018) show that microglial TREM2 is required for synaptic pruning in early development. TREM2-deficient mice show altered social behavior in adulthood, linking TREM2 to neurodevelopmental disease.
Insights
Microglial TREM2 (triggering receptor expressed on myeloid cells 2) is crucial for synaptic pruning during early development. TREM2 deficiency in mice leads to altered social behavior, suggesting a role in neurodevelopmental disorders.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Triggering receptor expressed on myeloid cells 2 (TREM2) is primarily known for its function in microglial phagocytosis.
- TREM2 is implicated in various neurodegenerative diseases.
Purpose of the Study:
- To investigate the role of microglial TREM2 in early neurodevelopment.
- To explore the consequences of TREM2 deficiency on brain function and behavior.
Main Methods:
- Utilized TREM2-deficient mouse models.
- Assessed synaptic pruning during early developmental stages.
- Evaluated social behavior in adult mice.
Main Results:
- Microglial TREM2 is essential for proper synaptic pruning in early development.
- TREM2-deficient mice exhibit abnormal social behavior in adulthood.
- These findings link TREM2 to neurodevelopmental processes.
Conclusions:
- TREM2 plays a critical, previously unrecognized role in synaptic pruning.
- Dysfunctional TREM2 may contribute to neurodevelopmental disorders with social behavior deficits.
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