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Schizophrenia is a severe disabling brain disease affecting about 1% of the world s population. Due to the dynamic nature of the peripheral blood transcriptome, understanding miRNAs gene expression signature in schizophrenia is a promising tool for discovery of disease-related biomarkers and biological pathways involved. This study aimed to identify specific miRNA signature characteristic for schizophrenia by using genome-wide miRNA expression profiling in patients with schizophrenia vs. healthy controls. In the current study, we examined miRNA gene expression changes applying cust m made LC Science miRNA expression profiling service, by using pooled whole blood-derived total RNA samples in order to evaluate possible miRNAs molecules associated with the disease. Here, we report experimental proof for a differentially down expressed miR-320a, miR-320b, miR-320d and miR-320c members. To elucidate the biological pathways implicated in schizophrenia, additionally we searched for the validated target genes of miR-320 gene family that might play a role in the regulation of schizophrenia susceptibility genes using miRWalk database. This analysis revealed experimentally validated targets with specific function in nervous system and development including RCOR1, AGO1, REST, and EZH2. Finally, our results suggested that differentially expressed miR-320 family members might be involved in schizophrenia molecular pathways.

While the pharmacology of Ginkgo biloba leaf extract has been studied extensively, little is known about the pharmacological potential of Ginkgo biloba seeds, although they contain similar active ingredients that are responsible for the therapeutic effects of the leaf extract. In this study we used 70%-methanol Ginkgo biloba kernel extract, quantified its bioactive constituents and tested their cytotoxic effect on two cancer cell lines, A2058 and HCT116, and the non-tumor cell line McCoy-Plovdiv. We studied the biological effect of the extract by real-time analysis in the xCELLigence system, WST-1 assay and LIVE/DEAD viability assay. We show that the extract significantly perturbed the viability of cancer cells in a concentration- and time-dependent manner. In contrast, non-cancerous McCoy-Plovdiv cells sustained their proliferation potential even at high concentrations of the extract. Therefore, we propose that the active constituents of the Ginkgo biloba endosperm extract may interact additively or synergistically to protect against cancer.

Background: Although Autism Spectrum Disorder (ASD) is considered a heterogeneous neurological disease in childhood, a growing body of evidence associates it with mitochondrial dysfunction explaining the observed comorbidities. Introduction: The aim of this study is to identify variations in cellular bioenergetics and metabolism dependent on mitochondrial function in ASD patients and healthy controls using peripheral blood mononuclear cells (PBMCs). We hypothesized that PBMCs may reveal the cellular pathology and provide evidence of bioenergetic and metabolic changes accompanying the disease. Method: PBMC from children with ASD and a control group of the same age and gender were isolated. All patients underwent an in-depth clinical evaluation. A well-characterized cohort of Bulgarian children was selected. Bioenergetic and metabolic studies of isolated PBMCs were performed with a Seahorse XFp analyzer. Result: Our data show that PBMCs from patients with ASD have increased respiratory reserve capacity (by 27.5%), increased maximal respiration (by 67%) and altered adaptive response to oxidative stress induced by DMNQ. In addition, we demonstrate а strong dependence on fatty acids and impaired ability to reprogram cell metabolism. The listed characteristics are not observed in the control group. These results can contribute to a better understanding of the underlying causes of ASD, which is crucial for selecting a successful treatment. Conclusion: The current study, for the first time, provides a functional analysis of cell bioenergetics and metabolic changes in a group of Bulgarian patients with ASD. It reveals physiological abnormalities that do not allow mitochondria to adapt and meet the increased energetic requirements of the cell. The link between mitochondria and ASD is not yet fully understood, but this may lead to the discovery of new approaches for nutrition and therapy.

Background: NGF is a molecule with a pleiotropic role, affecting neuro-immune functions, energy homeostasis, and synaptic plasticity. The mechanisms of NGF-induced neuronal differentiation are well established, but its effect on mitochondria in autism spectrum disorder (ASD) is still unclear. We hypothesize that NGF-induced neuronal development requires large amounts of energy, and mitochondria in ASD are overloaded to meet the new functional requirements. Method: The study includes primary diagnosed ASD children. Peripheral blood mononuclear cells (PBMCs) and plasma were obtained from both patients and typically developing children (TDC). PBMCs were analyzed with Seahorse XFp, and plasma NGF protein levels were measured. Results: We detected nearly 50% higher NGF levels and approximately 40% elevation in spare respiratory capacity in ASD compared to TDC. These findings are consistent with the observed difference in maximal respiration, which was also significantly higher in the patient group. Both mitochondrial respiration and NGF plasma levels exhibit a strong potential to discriminate children with ASD from TDC. Conclusions: This study is the first to link elevated NGF with mitochondrial respiration and altered energy homeostasis in ASD. High NGF correlates with basic bioenergetic signatures that may be used as a screening tool to improve early diagnosis and clinical follow-up in ASD.

MiRNAs are attractive candidates for ASD molecular biomarkers. show significant differential expression. MiR-424-5p and miR-500a-5p are the most dysregulated miRNAs in ASD patients. ROC analyses reveal miR-197-5p, miR-500a-5p and miR-424-5p as sensitive predictors. The combination of mir-500a-5p and mir-197-5p exhibits the highest diagnostic power.

Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder. It is characterized by the accumulation of α-Synuclein aggregates and the degeneration of dopaminergic neurons in substantia nigra in the midbrain. Although the exact mechanisms of neuronal degeneration in PD remain largely elusive, various pathogenic factors, such as α-Synuclein cytotoxicity, mitochondrial dysfunction, oxidative stress, and pro-inflammatory factors, may significantly impair normal neuronal function and promote apoptosis. In this context, neuroinflammation and autophagy have emerged as crucial processes in PD that contribute to neuronal loss and disease development. They are regulated in a complex interconnected manner involving most of the known PD-associated genes. This review summarizes evidence of the implication of neuroinflammation and autophagy in PD and delineates the role of inflammatory factors and autophagy-related proteins in this complex condition. It also illustrates the particular significance of plasma and serum immune markers in PD and their potential to provide a personalized approach to diagnosis and treatment.

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