LAUSR

Background The exposure to biological abnormalities proper of the psychiatric conditions (e.g. inflammation, oxidative stress, poor sleep and nutrition, insufficient exercise, cigarette smoking) may lead to accelerated cellular aging. Telomere length has been used as an index of biological aging in psychiatric illnesses and, using the same rationale, a novel age acceleration predictor is emerging: DNA Methylation Age (DMA). We tested the hypothesis that DMA could be associated with Schizophrenia (SCZ), its psychopathology and response to treatment in early stages of illness. Methods We assayed 60 antipsychotic-naive First Episode of Psychosis patients (FEP), the same individuals after 2-month risperidone-exclusive treatment and 59 Healthy Controls (HC), totaling 119 participants. Psychiatric diagnosis was assessed using the Semi-Structured Clinical Interview for DSM-IV Axis-I (SCID-I). We used the Positive And Negative Syndrome Scale (PANSS) to assess positive and negative symptoms and general psychopathology. We considered as risperidone-responders those with a decrease of at least 30% in PANSS. Telomere length was determined using a multiplex qPCR assay, whereas DNA methylation age was estimated by methylation levels at 353 genomic sites (Horvath, 2013) from Illumina 450 K methylation microarray. Results We found a correlation between chronological age and DMA (r2=0.899; p Discussion Our data shows that the DMA is highly correlated to chronological age but not to TL, suggesting DMA could be a better aging measure than TL. In addition, we showed that DMA does not associate with either symptoms or psychopathology, but may be associated with increased risk for schizophrenia in treatment naive patients.