The human-type consciousness (defined as ability of self-recognition) has high evolutionary advantage, but the complexity of its anatomical/neurochemical background makes it prone to disturbances. Schizophrenia is one of cognitive disorders, arising from deficits in neural connectivity and in neurotransmission. The neurochemical hypothesis points to the disturbances in dopaminergic transmission: hyperactivity in mesolimbic and striatal systems (responsible for positive symptoms) with concomitant hypofunction of mesocortical system (hypofrontality and negative symptoms). This poses difficulties for pharmacotherapy: dopaminergic receptor blockade abolishes positive, but may aggravate negative symptoms. Difference in serotonin control of various dopaminergic subsystems permits to overcome some difficulties. The neurodevelopmental hypothesis of schizophrenia underlies the role of prenatal and perinatal stress disturbing neuronal migration leading to disrupted cortical architecture. In neurodevelopmental disorders stress hormones are the wreckers and neurotrophins are protectants. A role for BDNF is suggested as its levels are decreased in schizophrenic brain and its Val66Met polymorphism is associated with earlier onset of the disease. The emergence of schizophrenia in late adolescence may be caused by inadequate BDNF supply at the time of final maturation of prefrontal cortex, and attempts of correction of BDNF level may be worth trying. It may be assumed that schizophrenia is the result of wrong interactions between stress, genetic and developmental factors. Studies on candidate genes for schizophrenia and of endophenotypes lead to better understanding of the disease and prospects for more efficient therapy. The question arises why the genes involved in schizophrenia had not been eliminated in the course of evolution?