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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Abstract
Schizophrenia (SZ) is a chronic neuropsychiatric
disorder characterized by affective, neuromorphological
and cognitive impairment, deteriorated social
functioning and psychosis with underlying molecular
abnormalities, including gene expression changes.
Observations have suggested that fasciculation and
elongation protein ζ-1 (FEZ1) may be implicated
in the pathogenesis of schizophrenia. Nevertheless,
our current knowledge of the expression of FEZ1 in
peripheral blood of schizophrenia patients remains
unclear. The purpose of this study was to identify
the characteristic gene expression patterns of FEZ1
in peripheral blood samples from schizophrenia patients.
We performed quantitative reverse-transcriptase
(qRT-PCR) analysis using peripheral blood from
drug-free schizophrenia patients (n = 29) and age and
gender-matched general population controls (n = 24).
For the identification of FEZ1 gene expression patterns,
we applied a comparative threshold cycle (CT)
method. A statistically significant difference of FEZ1
mRNA level was revealed in schizophrenia subjects
compared to healthy controls (p = 0.0034). To the
best of our knowledge, this study is the first describing
a down-regulation of FEZ1 gene expression in
peripheral blood of patients with schizophrenia. Our
results suggested a possible functional role of FEZ1
in the pathogenesis of schizophrenia and confirmed
the utility of peripheral blood samples for molecular
profiling of psychiatric disorders including schizophrenia.
The current study describes FEZ1 gene expression
changes in peripheral blood of patients with
schizophrenia with significantly down-regulation of
FEZ1 mRNA. Thus, our results provide support for
a model of SZ pathogenesis that includes the effects
of FEZ1 expression.
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