Testosterone and Depression

Androgens have various effects on human body and mood. Testosterone, a hormone mainly secreted from testes and adrenals, is one of the most potent androgens. Multiple studies have found that testosterone plays a role in regulating sexual activity, libido, social behaviors, aggression, cognitive functions, sleep control and well-being in men and women. Testosterone deficiency in hypogonadic or elderly men leads to neuropsychiatric problems, such as fatigue, loss of libido, irritability, insomnia and depressive mood. Testosterone replacement therapy consistently reverses these sequel in men. On the other hand, hyperandrogenic states in women are related to aggression and antisocial behavior, which might lead to depressive mood. Low testosterone levels may also result in depression among oophorectomized women. Because of such effects, a relationship between testosterone and depression has long been an issue of speculation, but yet very few studies have addressed this relation. Along with clinical studies, experimental and epidemiological studies show that testosterone is related to depression in men and women. But studies of testosterone concentrations in depression have yielded inconsistent results reporting low as well as high testosterone levels associated with depression. In this article, the physiological and psychological effects of testosterone and evidence regarding its relationship to depressive disorders and possible gender differences have been reviewed

Association of a haplotype in the NRG1 gene with schizophrenia: a case-control study

Schizophrenia (SZ) is a severe multifactorial disease. NRG1 is a gene acting in the development of SZ. A number of NRG1 single nucleotide polymorphisms (SNPs) and their haplotypes are associated with SZ. In the present study, we investigated the association of a NRG1 haplotype (G-C in rs6988339-rs3757930 frame) which was reported to be associated with SZ, and two other SNPs in the same gene (rs74942016, rs80127039) whose rare missense alleles were found in SZ patients. Also, we analyzed disease associations of potential new haplotypes constructed by the variants of these SNPs

EVALUATION OF BLOOD ZONULIN LEVELS, INFLAMMATORY PROCESSES AND NEURONAL CHANGES IN CHILDREN WITH AUTISM SPECTRUM DISORDER

Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by symptoms such as limited, and repetitive behavior patterns and disordered social interaction and communication. The etiology of Autism Spectrum Disorder (ASD) is not clearly known, it has been emphasized that the immune-inflammatory system may also play a role in this disease. This study aimed to evaluate in intestinal permeability, food antigen-antibody levels, inflammatory processes, and neuron damage in patients with ASD. Subjects and methods: Thirty-five chıldren between the ages of 3-12 with ASD and 35 controls were included in the study. Both participants\u27 height and weight were measured, and the parents filled the Socio-demographic Data and the Gastrointestinal Systems (GIS) Symptoms Form. Venous blood samples were collected, and serum zonulin, anti-gliadin Ig A and Ig G, IL6, TNF-alpha, TGFß, S100B, and NSE levels were measured by ELISA. Results: Serum zonulin levels in the ASD group were found to be significantly lower. IL-6 and TGF-ß were found to be significantly higher in the ASD group. There was no difference between the two groups in terms of serum anti-gliadin Ig A and Ig G and TNF-alpha values. Also, GIS symptoms, NSE and S100B levels were found similar between two groups. Conclusions: Although findings showing low zonulin levels and increased inflammatory processes in ASD were found in this study, no difference was found in the parameters of brain damage. The findings show that intestinal permeability does not decrease in ASD and that inflammatory processes may play a role in ASD