Semantic priming, the automatic activation of related concepts, is key to efficient cognition and language processing. In schizophrenia, particularly in positive thought disorder, this process is often disrupted, leading to hyperpriming (excessive activation) or hypopriming (reduced activation). These disruptions reflect a broader imbalance in the brain’s signal-to-noise ratio, where relevant signals are overwhelmed by noise. Dysfunction in dopamine D1 receptors and GABAergic interneurons contributes to this disinhibition, resulting in overly broad or disorganized semantic activation that complicates cognitive processing.

A neurobiological perspective links these semantic disruptions to broader cognitive impairments in schizophrenia. Studies highlight mechanisms such as reduced cortical inhibition and left hemisphere dysfunction, exacerbated by D1 and NMDA receptor hypofunction. These findings offer potential therapeutic pathways and emphasize the need for further research to understand how these neural disruptions influence symptoms like working memory deficits and language disturbances.

Reference: Almeida VN, Radanovic M. Semantic priming and neurobiology in schizophrenia: A theoretical review. Neuropsychologia. 2021;163:108058. doi: 10.1016/j.neuropsychologia.2021.108058.