Schizophrenia is a prevalent mental disorder characterized with typical symptoms include false beliefs, unclear or confused thinking, auditory hallucinations, reduced social engagement and emotional expression, and lack of motivation. As one of the mental diseases with extremely high incidence, the lifetime prevalence of schizophrenia worldwide is up to 1%. According to what people have known about schizophrenia, it has been generally accepted that the pathogenesis of schizophrenia is a combination of both genetic and environmental factors, and the latter accounts for a major role (heritability as high as 81%).

Although existing studies have reported many schizophrenia susceptible genes and single nucleotide polymorphisms (SNPs), the genetic basis and underlying mechanisms of schizophrenia are still far from clear. One of the assumptions is that the mitochondrial dysfunction is one of the reasons of the incidence of schizophrenia because human brain is the most energy-intensive human organ and it consumes 20%-25% of body's total energy consumption, whereas, the mitochondria is the powerhouse of cells. Therefore, there is no wonder why the relationship between mitochondrial and schizophrenia has aroused so extensive attentions.

To explore the potential association between mitochondrial complex I, the largest and the most complicated component of the respiratory chain, which plays a central role in electron transportation and schizophrenia, by collaborating Dr. CHEN Xiaogang (the Second Xiangya Hospital), the colleagues of Dr. YAO Yonggang (Kunming Institute of Zoology, CAS) conducted a comprehensive genetic association study by genotyping 46 tag SNPs from 7 nuclear-encoded genes of mitochondrial complex I in Han Chinese with and without schizophrenia and reanalysis of the Psychiatric Genetics Consortium (PGC) dataset.

The results showed that by using a rigorous statistical standard to avoid possible false positive results, no significant association between genetic polymorphisms from the 7 selected genes of mitochondrial complex I and schizophrenia were found, suggesting that these genes are unlikely to confer risk of schizophrenia in Han Chinese population. Moreover, no robust association between these SNPs and schizophrenia in the PGC data were observed either. In addition, the analyses to test if genetic variants of these 7 nuclear-encoded genes of mitochondrial complex I were associated with early onset schizophrenia (EOS, patients with a younger age of onset, usually below 18) in Han Chinese also showed up negatively. These findings suggest that common SNPs in the nuclear-encoded core subunit genes of mitochondrial complex I may not confer genetic susceptibility to schizophrenia

This study for the first time has systematically analyzed the genetic correlation between mitochondrial complex I and schizophrenia. The main findings have been published on Scientific Reports (http://www.nature.com/srep/2015/150608/srep11076/full/srep11076.html).