Table 2.
Cross-sectional studies.
| Model/Tissue | Method | Main Findings | Reference |
|---|---|---|---|
| Leukocytes of SCZ patients (n = 177) and controls (n = 171) | luminometric methylation analysis (LUMA) | • Increased global methylation in patients treated with haloperidol compared to other treatments | [49] |
| Saliva samples of SCZ (n = 30), first-degree relatives of SCZ (n = 15), controls (n = 30)/postmortem brain samples of patients with SCZ (n = 35) and BD (n = 35) | Quantitative methylation specific PCR | • Increased DNA methylation of DTNBP1 promoter in the saliva of patients with SCZ compared to controls • Inverse correlation between DTNBP1 methylation and expression in post-mortem brains of SCZ patients • Trend to reduced DNA methylation of DTNBP1 by antipsychotics treatment |
[79] |
| Postmortem brain samples of patients with BD (n = 35) and controls (n = 35) | Quantitative methylation specific PCR | • No significant difference of the DTNBP1 promoter region associated with antipsychotic treatment in patients with BD | [79] |
| Transformed lymphoblast cell lines from: lithium responders BD (n = 14), affected relatives (n = 14), unaffected relatives (n = 16), Healthy controls (n = 16) | ELISA | • Decreased DNA methylation in cell lines of BD patients, affected and unaffected relatives, compared to healthy controls • Lithium-induced decrease in global DNA methylation in BD patients (lithium responders) compared to controls |
[80] |
| Whole blood of patients with BD (n = 172), Human | Infinium Human-Methylation450 BeadChip | • Quetiapine, VPA showed significant DNA methylation alterations patients with BD | [81] |
| Peripheral blood from BD patients on Li monotherapy (n = 29), Lithium + VPA (n = 11), Lithium + antipsychotics (n = 21), healthy controls (n = 26) | ELISA | • Hypomethylation of DNA in BD patients treated with lithium monotherapy vs. lithium + VPA or healthy controls • No significant relation between DNA methylation and lithium response |
[82] |
| PBMC from BDI (n = 45), BDII (n = 49), and control subjects (n = 52) | Methylation-specific qPCR | • Decrease of DNA methylation at BDNF promoter I in patients with antidepressant therapy vs. controls • Decrease of DNA methylation at BDNF promoter I in patients with lithium therapy vs. other medications • Decrease of DNA methylation at BDNF promoter I in patients with VPA therapy vs. other medications |
[50] |
| PBMC from BDI (n = 45), BDII (n = 45) | methylation specific qPCR | • Decrease of DNA methylation at PDYN promoter I in patients with lithium or VPA therapy (n = 25) vs. other medications | [83] |
| PBMC from BDI (n = 61), BDII (n = 50), MDD (n = 43) patients | methylation specific qPCR | • Not significant trend for a decrease of DNA methylation in patients treated with lithium and VPA | [84] |
| PBMC from MDD (n = 207), BD (n = 59) and controls (n = 278) | Methylation-specific quantitative PCR | • BDNF gene exon I promoter methylation increased in MDD compared to BD and controls • Increased BDNF DNA methylation in MDD patients associated with antidepressant therapy |
[85] |
| Peripheral leukocytes from MDD patients (10 best responders and 10 worst responders to paroxetine) | Infinium Human-Methylation450 BeadChip | • Methylation levels of the CpG sites in PPFIA4 and HS3ST1 gene can discriminate between best and worst responders | [86] |
ELISA (Enzyme-Linked Immunosorbent Assay), Polymerase Chain reaction (PCR), quantitative PCR (qPCR), Bipolar disorder type 1 (BDI), Bipolar disorder type 2 (BDII).