BackgroundThe incidence rate of schizophrenia about 1 percent in the world.Disturbances in 5-HT neurotransmission have been indicated as biological substrates in several psychiatric disorders, including schizophrenia.By determining magnitude and duration of 5-HT synaptic signal, serotonin transporter (5-HTT) plays a key role in the regulation of serotonergic neurotransmission.Rcent reserch demonstrate that methylation at this CpG island is associated with decreased levels of 5HTT mRNA.The serotonin transporter is thought to be the principal regulator of serotonergic activity.Therefore epigenetic effects at this locus are thought to be important moderators of vulnerability to schizophrenia.ObjectivesTo quantitatively evaluate the CpG island methylation status in serotonin transporter promoter region and analyses its role in the etiological of schizophrenia.Materials and MethodWithdrawal Peripheral blood from 30 primary schizophrenias, Using a bisulphate genomic sequencing to detect their CpG island methylation status in 5-HTT promoter region. ResultsThere was no significant difference in the schizophrenia patients methylation rates and healthy controls (χ2=0.61, P>0.05); In addition, no significant methylation rates association was found at onset age of schizophrenia between 18-27 years old (χ2=1.00, P>0.05) and 28-42 years old (χ2=0.52,P>0.05);No significant methylation rates association was found between male(χ2=0.25, P>0.05)and female(χ2=0.26,P>0.05)ConclusionWe demonstrate that methylation at this CpG island is not associated with the etiological of schizophrenia.
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