Review articleSynapse pathology and translational applications for schizophrenia

- Polygenic genetic variations contribute to the risk of schizophrenia.
- Aberrant synaptic signaling contributes to the pathophysiology of schizophrenia.
- Synaptic molecules are candidates for a novel therapeutic strategy for schizophrenia.

Schizophrenia is a chronic, severe, and disabling brain disorder, with an estimated lifetime prevalence of 0.7%. Despite its relatively low prevalence, the onset of schizophrenia usually occurs early in life, resulting in a severe lifelong disability for patients and increasing the economic and care burden on their families. This makes schizophrenia one of the most catastrophic mental illnesses. Although the etiology of schizophrenia remains poorly understood, clinical, genetic, and pharmacological studies have indicated that its pathophysiology involves synaptic disturbances. Here, I review the evidence suggesting synaptic disturbance as the causal pathophysiology of schizophrenia and discuss the possible application of synaptic intervention as a novel therapeutic strategy for schizophrenia.