Deletion of Mex3c Gene Leads to Autistic-Like Behavior in Mice by Inhibiting AMPK Signal Pathway

Hui CaiKai Wang^*

• Ningxia Medical University, Yinchuan, China

Autism Spectrum Disorder (ASD), a hereditary neurodevelopmental condition, is significantly influenced by genetic changes, particularly in ASD risk genes. These alterations disrupt transcription and signaling, affecting neural development (e.g., cell growth, synapse formation/adaptability) and correlating with the severity of social impairment symptoms. Eliminating the Mex3c gene leads to a cascade of metabolic alterations, impacting energy balance and development. Our initial investigations into the function of Mex3c in nervous system development have shown that deleting the Mex3c gene not only leads to abnormalities in neural tube formation in mouse babies but also has negative effects on their cognitive and emotional regulation. Thus, we postulated that Mex3c may serve as a novel susceptibility gene for ASD. To determine if Mex3c deletion represents a new contributing factor to ASD, a set of experimental arrangements was created. The findings indicated that the elimination of the Mex3c gene resulted in autistic-like behavior in mice, a decrease in the number of neurons and a deterioration in synaptic connections and their ability to change and adapt.Further, Mex3c gene knockout increased AMPK protein levels, disrupting the AMPK/SIRT1/PGC1a signaling pathway, resulting in abnormal mitochondrial structure and function. In conclusion, the Mex3c gene regulates the AMPK/SIRT1/PGC1a signaling pathway, and disruption or changes in this gene have been associated with the onset of autism. This association may occur through the inhibition of the AMPK/SIRT1/PGC1a signaling pathway.