Abstract
Dysbindin gene is currently considered to be a candidate gene for schizophrenia. Dysbindin is a part of BLOC-1, which is involved in a vesicle transport.
It is supposed that dysbindin presynaptically participates in the exocytosis of glutamate and influences long-term potentiation and neuronal synaptoplasticity. It exerts an anti-apoptotic effect possibly via PI3K/PDK1/Akt signalling pathway.
In schizophrenia patients, reduced expression was found in dorsolateral prefrontal cortex and hippocampal formation, leading to decreased glutamate and presumably also dopamine release and thus modifying information transmission in these areas. It is presumed that reduced dysbindin expression affects negatively cognitive functions and negative symptoms severity in schizophrenia.