Genetic basis of schizophrenia: Basic hypothesis pathways and gene functions

Abstract

Correspondence: Alper Tanrıkulu. Deneysel Tıp Enstitüsü, 41470 Gebze-Kocaeli, Türkiye. e-mail: tanriklualper@gmail.com ABSTRACT Schizophrenia is a neurodegenerative disease in which cognitive and behavioral disorders coexist. Based on magnetic resonance imaging (MRI) studies, there are problems in neuron connections and the prefrontal lobe is almost completely disrupted. It is highly inherited. Genome scans have shown that variations in the major histocompatibility complex (MHC) genes may be a risk factor for schizophrenia. Detection of the differences in allele frequency is also important in the etiology studies of the disease. Schizophrenia is a very complex disease due to dysfunction of almost entire neurocognitive related systems. With the discovery of antipsychotic drugs, many hypotheses have been put forward on the etiology of the disease. One of them is dopamine hypothesis of schizophrenia and the other is glutamate hypothesis of schizophrenia. Antipsychotic drugs alleviate psychosis symptoms by interacting with protein receptors or ion channels involved in dopamine glutamate and gamma aminobutyric acid (GABA) pathways. In this review, we discuss dopamine and glutamate hypotheses based on the etiology of schizophrenia and the genes that have the most evidence for their relationship with the disease.