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Tryptophan catabolites pathway disorders are observed in patients with depression. Moreover, single nucleotide polymorphisms of tryptophan hydroxylase genes may modulate the risk of depression occurrence. The objective of our study was to confirm the association between the presence of polymorphic variants of TPH1 and TPH2 genes, and the development of depressive disorders. Six polymorphisms were selected: c.804‐7C>A (rs10488682), c.‐1668T>A (rs623580), c.803+221C>A (rs1800532), c.‐173A>T (rs1799913)—TPH1, c.‐1449C>A (rs7963803), and c.‐844G>T (rs4570625)—TPH2. A total of 510 DNA samples (230 controls and 280 patients) were genotyped using TaqMan probes. Among the studied polymoorphisms, the G/G genotype and G allele of c.804‐7C>A—TPH1, the T/T homozygote of c.803+221C>A—TPH1, the A/A genotype and A allele of c.1668T>A—TPH1, the G/G homozygote and G allele of c.‐844G>T—TPH2, and the C/A heterozygote and A allele of c.‐1449C>A—TPH2 were associated with the occurrence of depression. However, the T/T homozygote of c.‐1668T>A—TPH1, the G/T heterozygote and T allele of c.‐844G>T—TPH2, and the C/C homozygote and C allele of c.‐1449C>A—TPH2 decreased the risk of development of depressive disorders. Each of the studied polymorphisms modulated the risk of depression for selected genotypes and alleles. These results support the hypothesis regarding the involvement of the pathway in the pathogenesis of depression.

Background: Neuroplasticity ensures the improvement of functional status in patients after stroke. The aim of this study was to evaluate the effect of extremely low-frequency electromagnetic field therapy (ELF-EMF) on brain plasticity in the rehabilitation of patients after stroke.Methods: Forty-eight patients were divided into two groups underwent the same rehabilitation program, but in the study group, the patients additionally were exposed to a standard series of 10 ELF-EMF treatments. To determine the level of neuroplasticity, we measured the plasma level of the brain-derived neurotrophic factor (BDNF), the vascular-endothelial growth factor, as well as BDNF mRNA expression. Additionally, we determined the molecule levels for hepatocyte growth factor, stem cell factor, stromal cell-derived factor 1α, nerve growth factor β, and leukemia inhibitory factor, using 5plex cytokine panel in plasma. After 4 weeks, during which patients had undergone neurorehabilitation and neurological examinations, we assessed functional recovery using the Barthel Index, Mini-Mental State Examination (MMSE), Geriatric Depression Scale, National Institutes of Health Stroke Scale (NIHSS), and the modified Rankin Scale (mRS).Results: We observed that ELF-EMF significantly increased growth factors and cytokine levels involved in neuroplasticity, as well as promoted an enhancement of functional recovery in post-stroke patients. Additionally, we presented evidence that these effects could be related to the increase of gene expression on the mRNA level. Moreover, a change of BDNF plasma level was positively correlated with the Barthel Index, MMSE, and negatively correlated with GDS.Conclusion: Extremely low-frequency electromagnetic field therapy improves the effectiveness of rehabilitation of post-stroke patients by improving neuroplasticity processes.

The dominating hypothesis among numerous hypotheses explaining the pathogenesis of depressive disorders (DD) is the one involving oxidative and nitrosative stress. In this study, we examined the association between single-nucleotide polymorphisms of the genes encoding SOD2 (superoxide dismutase 2), CAT (catalase), GPx4 (glutathione peroxidase 4), NOS1 (nitric oxide synthase 1), NOS2 (nitric oxide synthase 2), and the development of depressive disorders. Our study was carried out on the DNA isolated from peripheral blood collected from 281 depressed patients and 229 controls. Using TaqMan probes, we genotyped the following six polymorphisms: c.47T>C (p.Val16Ala) (rs4880) in SOD2, c.-89A>T (rs7943316) in CAT, c.660T>C (rs713041) in GPx4, c.-420-34221G>A (rs1879417) in NOS1, c.1823C>T (p.Ser608Leu) (rs2297518), and c.-227G>C (rs10459953) in NOS2. We found that the T/T genotype of the c.47T>C polymorphism was linked with an increased risk of depression. Moreover, the T/T genotype and T allele of c.660T>C increased the risk of DD occurrence, while the heterozygote and C allele decreased this risk. On the other hand, we discovered that the A/A genotype of c.-89A>T SNP was associated with a reduced risk of DD, while the A/T genotype increased this risk. We did not find any correlation between the genotypes/alleles of c.-420-34221G>A, c.1823C>T, and c.-227G>C, and the occurrence of DD. In addition, gene-gene and haplotype analyses revealed that combined genotypes and haplotypes were connected with the disease. Moreover, we found that sex influenced the impact of some SNPs on the risk of depression. Concluding, the studied polymorphisms of SOD2, CAT and GPx4 may modulate the risk of depression. These results support the hypothesis that oxidative and nitrosative stresses are involved in the pathogenesis of depressive disorders.

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