Medicus, Vol. 32 No. 1. Psihoze, 2023.
Review article
Neurobiology of Schizophrenia
Aleksandar Savić
Abstract
The complexity of disorders in the schizophrenia spectrum thwarted the emergence of simple unified biological models that would explain the concrete mechanism of their occurrence. However, from the inception of the disorders, distinct structural changes have been identified in patients’ brains. We see an overall loss of volume and enlargement of the cerebral ventricles, which also showed a longitudinal dynamic with certain predictive value. Some volume changes in the gray matter are also associated with specific symptoms. Although several neurochemical theories of psychotic disorders exist, the theory of dopamine dysfunction (hyperdopaminergia) in the mesolimbic pathway still dominates and explains the emergence of positive symptoms of psychosis and the therapeutic effect of dopamine D2 receptor blockers. The glutamate theory based on the possible dysfunction of glutamate NMDA receptors, and the inflammatory theory explain certain mechanisms that may precede dopamine dysfunction as the “final common path” to psychosis. Nothing displays the complexity of the disorder as much as data on gene loci as a risk for developing schizophrenia. Research, in accordance with the generally accepted polygenic model of the disorder, has identified more than 100 risk-related loci, including those encoding essential components of dopamine and glutamate neurotransmission. It is interesting that loci on the 6th chromosome associated with immune response confirm the inflammation model. It sees ITUs and other infections as blows to the already vulnerable system that leads to dysfunction and the emergence of disorders. According to accepted models, disorders exist prenatally and circumstances in life bring about its emergence.
Keywords
schizophrenia; psychosis; neuroanatomy; dopamine; glutamate; inflammatory theory
Hrčak ID:
308608
URI
Publication date:
9.10.2023.
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