The Role of Genetic Mutation on Schizophrenia: A Basic Review Prior to Pharmacogenomics Dhea Nur Hikmah1, Alfian Syarifuddin1, Setiyo Budi Santoso1, Ratna Wijayatri1, Imron Wahyu Hidayat1,a
1Department of Pharmacy, Universitas Muhammadiyah Magelang, Indonesia
Abstract
A bioinformatical approach used to find indications for drug repositioning to produce new treatment paradigms for schizophrenia by comparing the binding profiles of currently available clinical compounds to targets or sets of targets derived from genome-wide association studies (GWAS) or other genetic studies. Here in, we present the molecular expression of schizophrenia due to polymorphism. The study involves literatures indexed by Scopus, and the search uses a combination of the following keyword variants- ^GWAS^ AND ^genom^, ^GWAS^ AND ^repurposing drug^. This study only used original articles in english which were peer reviewed journals published during 2022. Thus, the screening results of library sources were narrowed to 5 original articles papers that met the inclusion criteria. Our review shows that the primary hub gene from this module, SCN2B, is a well-known target of zonisamide, an antiepileptic and antiparkinsonian drug. SCN2B encodes for the voltage-gated sodium channel beta-2 subunit, which interacts covalently with the pore-forming alpha subunits to regulate activity. The remaining SynGO hub genes, SYNGR1, DNM1, and CAMK2A, are involved in the synaptic vesicle cycle. The gene DNM1 encodes Dynamin 1, a GTPase involved in synaptic vesicle endocytosis. SYNGR1 encodes synaptogyrin 1, a synaptic vesicle membrane component that regulates the synaptic vesicle cycle. Our findings give up new opportunities for the development of pharmacogenomic-based follow-up studies on racial variations that have not previously been studied.
