INVESTIGATION OF FASCICULATION AND ELONGATION PROTEIN ζ-1 (FEZ1) IN PERIPHERAL BLOOD REVEALS DIFFERENCES IN GENE EXPRESSION IN PATIENTS WITH SCHIZOPHRENIA
Vachev TI1, Stoyanova VK, Ivanov HY, Minkov IN, Popov NT
*Corresponding Author: Associate Professor Vili K. Stoyanova, M.D., Ph.D., Department of Pediatrics and Medical Genetics, Medical University ‒ Plovdiv, 15A Vasil Aprilov St., 4000 Plovdiv, Bulgaria. Tel: +359-32- 602-431; Fax: +359-32-602-593. E-mail: vi1sto@abv.bg
page: 31

INTRODUCTION

Schizophrenia (SZ) is a severe mental disorder affecting approximately 1.0% of the human population worldwide [1]. Twin, family and adoption studies strongly support that genetic factors play an important role in the etiology of SZ. Currently, numerous genetic studies, including linkage scans and their meta-analyses, candidate gene association analyses, gene expression and genome-wide association studies (GWAS) have identified particular genes and chromosomal loci with the disorder [2-4]. Circulating blood is easily accessible material and has been suggested as an alternative to tissue samples for molecular profiling of human disease and disease risk [3,5]. This is based on the capacity of peripheral blood to reflect pathological changes in the body. As the brain tissue is not easily accessible for investigation, blood-based expression profiling is increasingly being undertaken to search potential biomarkers for SZ [6,7]. Fasciculation and elongation protein ζ-1 (FEZ1) is one of the first identified binding partners of Disrupted-in Schizophrenia 1 (DISC1), a susceptibility gene for major mental disorders including SZ in yeast two-hybrid screen of an adult human brain library [8]. Moreover, proteomic techniques revealed that FEZ1 protein interacts with various intracellular partners, such as motor signaling, and structural proteins, one of which is DISC1 [9]. Currently, the role of FEZ1 in mammalian neuronal development in vivo is not well understood. The FEZ1 null mice exhibit hyperactivity and enhanced responsiveness to psychostimulants [10], supporting a po-tential contribution of FEZ1 dysfunction to SZ. Recently, additional evidence based on sequencing of DISC1-interacting partner genes including FEZ1 revealed an increased burden of rare missense variants in SZ susceptibility in an isolated northern Swedish population [11]. In contrast, the FEZ1 gene shows no association to SZ in Caucasian or African American populations [12]. However, no association was found in either population between specific haplotypes and any of the psychiatric disorders [13]. Interestingly, there is a significant reduction of FEZ1 mRNA in both hippocampus and dorsolateral prefrontal cortex of SZ patients and also an association of the DISC1 genotype and FEZ1 mRNA levels [9]. All these findings raise the possibility that FEZ1 and DISC1 may assist in regulating both neuronal development and risk for SZ. We hypothesized that previously shown FEZ1 mRNA levels in prefrontal cortex of SZ patients may be relevant to those in peripheral blood tissue. The aim of this study was to identify gene expression patterns of FEZ1 in peripheral blood samples from SZ patients.



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