Abstract
Schizophrenia is a common psychiatric disorder that usually develops during adolescence and young adulthood. Since genetic and environmental factors are involved in the disease, the molecular status of the pathology of schizophrenia differs across patients. Recent genetic studies have focused on the association between schizophrenia and the immune system, especially microglia–synapse interactions. Microglia physiologically eliminate unnecessary synapses during the developmental period. The overactivation of synaptic pruning by microglia is involved in the pathology of brain disease. This paper focuses on the synaptic pruning function and its molecular machinery and introduces the hypothesis that excessive synaptic pruning plays a role in the development of schizophrenia. Finally, we suggest a strategy for diagnosis and medication based on modulation of the interaction between microglia and synapses. This review provides updated information on the involvement of the immune system in schizophrenia and proposes novel insights regarding diagnostic and therapeutic strategies for this disease.
Highlights
Microglia have been suggested to play a significant role in excessive synaptic elimination with respect to the pathology of schizophrenia
Recent publications indicating the contribution of complement components to schizophrenia are attracting attention with respect to this relationship
The monitoring and modulation of microglial synaptic pruning based on the complement system would be powerful tools for diagnosis and medication in schizophrenia
Summary
It is noteworthy that the major histocompatibility complex (MHC) locus located on chromosome 6 displayed a higher association with schizophrenia than any other locus across the genome, which is consistent with the findings of previous reports [14,15,16,17] This region contains genes related to innate immunity. In the Wisconsin Card Sorting Test, which assesses the flexibility of thinking associated with the PFC, a higher frequency of perseverative responses has been observed in patients with schizophrenia [31] Such functional disturbances in the PFC are consistent with the evidence from functional magnetic resonance imaging studies indicating the lower activity of the PFC with respect to episodic encoding and retrieval [33], and in response to consummatory pleasure [34]. Afterwards, we provide a novel insight into the diagnosis and treatment of schizophrenia based on microglia–synapse interactions
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