Schizophrenia has a strong genetic basis, although no single mutation causes the disease. Variations in the noncoding regions of DTNBP1, which encodes dysbindin, are associated with an increased risk of schizophrenia, and dysbindin expression is reduced in prefrontal cortex and hippocampus of schizophrenics. Dysbindin is part of a large endosomal protein complex called the “biogenesis of lysoso...

Dystrobrevin-binding protein 1 (DTNBP1), a gene encoding dysbindin-1, has been identified as a susceptibility gene for schizophrenia. Functioning with partners in synapses or the cytoplasm, this gene regulates neurite outgrowth and neurotransmitter release. Loss of dysbindin-1 affects schizophrenia pathology. Dysbindin-1 is also found in the nucleus, however, the characteristics of dysbindin in...

Genetic epidemiological studies suggest that individual variation in susceptibility to schizophrenia is largely genetic, reflecting alleles of moderate to small effect in multiple genes. Molecular genetic studies have identified several potential regions of linkage and two associated chromosomal abnormalities, and evidence is accumulating in favour of several positional candidate genes. Current...

Chronic mental diseases (CMD) like the schizophrenias are progressive diseases of heterogenous but poorly understood biological origin. An imbalance in proteostasis is a hallmark of dysfunctional neurons, leading to impaired clearance and abnormal deposition of protein aggregates. Thus, it can be hypothesized that unbalanced proteostasis in such neurons may also lead to protein aggregates in sc...

No effective drugs are currently available for the treatment of mental diseases, primarily because the underlying mechanism of mental diseases have not been adequately explored at the molecular level. However, recent studies have examined several molecular cascades whose disturbances are associated with mental diseases such as schizophrenia, bipolar disease and major depression. The most common...