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Epigenetic aberrations may serve as biomarker for schizophrenia

A highly significant hypomethylation was observed in individuals with schizophrenia, according to recent results.

Although schizophrenia has a strong hereditary component, departures from simple genetic transmission are prominent. DNA methylation has emerged as an epigenetic explanatory candidate of schizophrenia’s nonmendelian characteristics. To investigate this assumption, researchers examined genome-wide (global) and gene-specific DNA methylation levels, which are associated with genomic stability and gene expression activity, respectively.

Researchers in Sweden gathered DNA from leukocytes of patients with schizophrenia and controls. Individuals with schizophrenia demonstrated highly significant hypomethylation, according to global methylation results (P<2.0×10^-6). Results of a linear regression model indicated that antipsychotic treatment and disease onset explained 11% of the variance in global methylation (adjusted R²=0.11, ANOVA P<.001).

A link between haloperidol and higher — or control-like — methylation was observed (P=.001). Early onset, which the researchers noted was a “putative marker of schizophrenia severity,” was linked to lower methylation (P=.002).

Gene-specific methylation analyses also were conducted. Patients with schizophrenia demonstrated hypermethylation in the region of S-COMT (P=.004), which was in accordance with the dopamine hypothesis of psychosis.

“These data support the notion of a dysregulated epigenome in schizophrenia, which, at least globally, is more pronounced in early-onset patients and can be partly rescued by antipsychotic medication,” researchers wrote. “Blood DNA-methylation signatures show promise of serving as a schizophrenia biomarker in the future.”