The FADS2 gene encodes a key, rate-limiting enzyme involved in polyunsaturated fatty acid (PUFA) metabolism. Recent studies suggest that changes in plasma PUFA levels can lead to disruptions in the neurotransmission system and increase the risk of mood disorders. FADS2 variations may contribute to the individual risk of developing bipolar disorder (BD). We investigated the association of regulatory FADS2 rs28456 with BD in the Turkish population. We performed TaqMan genotyping on 100 patients with BD and 91 healthy controls. Our results did not show significantly different genotype or allele frequencies of rs28456 in the BD cases compared to controls. However, we stratified the cases based on family history, which revealed that minor rs28456-G was observed more frequently (P=0.056) in cases without a family history of psychiatric illness compared to those with a family history of psychiatric illness. A marginally significant difference in the distribution of the ?G? allele (P=0.053) between male patients and healthy males without a family history was observed. Our findings did not provide strong evidence supporting the reported association between rs28456 and BD, yet they point to its potential gender-specific effect, which requires further investigation. Future studies are necessary to explore the impact of FADS2 variations on BD risk in larger study groups, considering their potential interaction with non-inherited risk factors.

Background: Translocator Protein (TSPO) is a transmembrane protein located in the mitochondrial outer membrane and highly expressed in the brain, which makes it a potential biomarker for microglial activation and neuroinflammation in neurodegenerative diseases. However, its role in neuropsychiatric disorders and its contribution to methamphetamine (METH) addiction (MA) remain unclear. Here, we aimed to investigate the association of the TSPO rs6971 with susceptibility to MA and METH-associated psychosis (MAP) and to evaluate its effect on TSPO expression. Methods: We investigated the association of TSPO/rs6971 (Ala147Thr) with susceptibility to MA and METH-associated psychosis (MAP). Genotyping was performed on 300 individuals, including 200 diagnosed with METH use disorder, with 100 of these exhibiting MAP, along with 100 healthy controls (HCs). We explored how different genotypes influence TSPO expression at both the transcript and protein levels using RT-qPCR and ELISA. Results: Age- and sex-adjusted logistic regression analysis revealed nominal associations between the rs6971 AA genotype and MAP under the recessive and co-dominant genetic models, with stronger associations observed after excluding individuals with a family history of psychiatric disorders. Within the MAP group, carriers of the A allele exhibited increased circulating TSPO levels compared to those with the GG genotype. Additionally, higher protein concentrations (p = 0.036) were observed in heterozygous individuals with MAP, compared to METH users without psychosis. Conclusions: Our findings suggest that the expression of TSPO may be influenced by genotype, with A allele carriers showing elevated TSPO expression. Overall, these exploratory findings suggest potential for TSPO-based translational strategies for patients with MA, and highlight the need for more comprehensive evaluations in future research.

Schizophrenia is a common and complex psychiatric disorder with symptoms that significantly affect public health. Candidate gene studies reported that variants in genes involved in molecular processes associated with schizophrenia such as glutamatergic, dopaminergic, and GABAergic signaling pathways increase the risk of schizophrenia. Yet, the data obtained so far are incomplete for the development of new translational medicine approaches. Although the current research has promising results, it is still insufficient for the development of early diagnosis and treatment methods for schizophrenia management. Recent studies have reported that microRNAs detected in brain tissue and body fluids are differentially expressed in schizophrenia patients and control groups may be related to the etiology of schizophrenia. Although the determination of microRNA profiles associated with schizophrenia pathophysiology is very important for the development of new molecular approaches in the early diagnosis and treatment of the disease, the literature is still lacking in this field. Studies reporting schizophrenia-associated microRNAs in the existing literature have some limitations and methodological differences. In this review, we extracted the studies investigating the relationship between schizophrenia and microRNA in the last ten years and it was revealed that sample selection and microRNA detection methods are very important in terms of obtaining consistent results. Non-invasive detection of microRNAs expressed in the brain may have promising results for schizophrenia management. In this context, after a comprehensive literature search, miR-124-3p, miR-16-5p, and miR-34a-5p, which are differentially expressed in schizophrenia patients in the brain and blood, were prioritized as potential epigenetic biomarkers for schizophrenia. Our study provides data that can be utilized for translational medicine approaches to alleviate the burden of the disease in the community.