Relationship between Trem2 expression and VPA-Induced Autism Mice Model

Objective: Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social impairment, language disorder and repetitive behaviors. Recent studies have focused on the critical role of immune dysregulation and neuroinflammation in ASD pathophysiology. Triggering receptor expressed on myeloid cells 2 (Trem2), a microglial surface receptor involved in immune response modulation and phagocytosis, has emerged as a potential mediator of neuroinflammatory processes. Valproic acid (VPA) is known as an antiepileptic drug and used to form autism models in mice. In this study, we investigated the expression of Trem2 in the brains of valproic acid (VPA)-induced autism model mice.  

Materials and Methods: The VPA is administered 14 days after the mouse is born to induce autism-like phenotypes. Balb-C mice were used as the control group. Hippocampus tissue was taken from the 14-day of the groups and then total RNA was isolated. The expression level of Trem2 was evaluated by using quantitative Real-Time PCR (qRT-PCR). 

Results: Behavioral experiments showed ASD-like behaviors in VPA-induced autism models. Molecular analysis revealed the dysregulation of Trem2 expression in the hippocampus.  

Conclusion: These findings suggest that Trem2 may contribute to the neuroimmune alterations observed in ASD and could be a potential biomarker or therapeutic target in autism-related neuroinflammation. 

Acknowledgments: This study was conducted at Erciyes University Genome and Stem Cell Center, Genome and Transgenic Unit (GENKOK).  

Keywords: ASD, VPA, Trem2, neuroinflammation, hippocampus