<b><i>Background:</i></b> Patients suffering from schizophrenic psychosis show reduced synaptic connectivity compared to healthy individuals. Furthermore, the use of cannabis often precedes the onset of schizophrenic psychosis. Therefore, we investigated whether consumption of cannabis has an impact on the methylation pattern of schizophrenia candidate genes concerned with the development and preservation of synapses and synaptic function. <b><i>Methods:</i></b> Fifty blood samples of outpatients affected by treatment-resistant schizophrenic psychosis were collected in the outpatient department of Ch Ste Anne/INSERM (Paris, France). Extracted DNA was sent to the LMN/MHH (Hanover, Germany) where DNA samples were bisulfite converted. The methylation patterns of the promoter region of neuregulin 1 (<i>NRG1</i>), neurexin (<i>NRXN1</i>), disrupted in schizophrenia 1 (<i>DISC1</i>), and microtubule-associated-protein tau (<i>MAPT</i>) were then analysed by sequencing according to Sanger. <b><i>Results:</i></b> In <i>NRXN1</i> the group of non-consumer patients showed a methylation rate slightly lower than controls. In patients with preliminary use of tetrahydrocannabinol (THC) the <i>NRXN1</i> promoter turned out to be methylated almost two times higher than in non-consumer patients. In <i>MAPT</i>, non-consumer patients showed a significant lower mean methylation rate in comparison to controls. In THC-consuming patients the difference compared with controls became less. <i>NRG1</i> and <i>DISC1</i> showed no significant differences between groups, whereas <i>DISC1</i> appeared to be not methylated at all. <b><i>Conclusion:</i></b> In <i>MAPT</i> and <i>NRXN1</i> mean methylation rates were lower in non-consumer patients compared with controls, which seems to be a compensatory mechanism. With consumption of THC, mean methylation rates were increased: in the case of <i>MAPT</i> compared with controls, and in <i>NRXN1</i> even significantly beyond that. Methylation of <i>NRG1</i> and <i>DISC1</i> seems not to be affected by the psychiatric disorder or by consumption of THC.

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