Table 3.
Model/Tissue | Method | Main Findings | Reference |
---|---|---|---|
Peripheral blood of patients with SCZ (n = 82) | Bisulfite conversion + PCR + pyrosequencing | • Decreased DNA methylation at CpG13 of HTR1A associated with poorer response to antipsychotics | [87] |
Peripheral blood from SCZ patients (n = 21) | Infinium Human-Methylation450 BeadChip | • Clozapine-induced DNA methylation changes in the CREBBP gene were significantly correlated with clinical improvements | [88] |
Peripheral blood from SCZ patients; good responders (n = 88), poor responders (n = 54) | Methylation-specific PCR + mass spectrometry | • Seven CpGs at CYP3A4 and CYP2D6 genes were differentially methylated in good vs. poor responders to risperidone therapy | [89] |
Peripheral blood from SCZ patients n = 20 (12 M/8 F) | MeDIP ChIP | • Before treatment: nine genes with DMR in male SCZ patients in complete remission after treatment (vs. matched control subjects) • After treatment: six genes with DMR in male SCZ patients in complete remission after treatment (vs. matched control subjects) • Before treatment: one gene (M1R181C) with DMR in female SCZ patients in complete remission after treatment (vs. matched control subjects) • After treatment: one gene (BCOR) with DMR in female SCZ patients in complete remission after treatment (vs. matched control subjects) |
[90] |
Leukocytes from patients with MDD (n = 108) | Bisulfite conversion followed by PCR | • Increased of SLC6A4 DNA methylation level associated with impaired treatment response to antidepressants | [91] |
Whole blood from patients with MDD (n = 50 before treatment and n = 40 after 6 weeks of treatment) and controls (n = 50) | Methylation-specific PCR + mass spectrometry | • Methylation level of the third CpG site of SLC6A4 gene association with better therapeutic response to antidepressant therapy in patients MD | [92] |
Whole blood from patients with MDD (n = 94), (Human) | Bisulfite conversion + PCR | • Increased DNA methylation of SLC6A4 gene associated with better treatment response to escitalopram | [93] |
Whole blood from patients with MDD, (n = 61) (Human) | Bisulfite conversion + PCR | • No major influence of mono amino oxidase (MAO-A) gene methylation status on escitalopram response | [94] |
Peripheral blood of patients with MDD (n = 85) | Bisulfite sequencing | • Significant association of 668 CpG sites of HTR1A and 1401 CpG sites of HTR1B gene methylation with treatment response to escitalopram | [95] |
Peripheral blood samples of patients with MDD treated with escitalopram (n = 80) or nortriptyline (n = 33) | Bisulfite conversion + PCR | • Fourth CpG island hypomethylation of IL-11 gene associated with better response to nortriptyline • Hypermethylation of fourth CpG island of IL-11 gene associated with better response to escitalopram |
[96] |
Polymerase Chain reaction (PCR), quantitative PCR (qPCR), Methylated DNA Immunoprecipitation (MeDIP), Chromatin ImmunoPrecipitation (ChIP).