
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
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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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