Neuronal Aralar/AGC1 deficiency impairs social behavior through dopaminergic and redox dysfunction and is rescued by β-hydroxybutyrate
Background: Pathogenic variants in SLC25A12/AGC1 (Aralar) have been linked to autism spectrum disorder (ASD), yet the mechanisms connecting neuronal metabolic dysfunction to altered social behavior remain poorly understood. Aralar is a key component of the malate-aspartate shuttle, supporting neuronal oxidative metabolism and lactate utilization. Here, we investigated the consequences of…
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