Schizophrenia is a complex psychiatric disorder with a multifactorial etiology involving genetic, neurodevelopmental, environmental, and socio-cultural factors[8]. The neurobiology of schizophrenia remains largely incomplete, but several key findings have emerged: 1. Dopaminergic dysfunction: There is strong evidence implicating dysfunction of dopaminergic neurotransmission, particularly in the striatum and prefrontal cortex, in the genesis of psychotic symptoms[3][11]. 2. Glutamatergic and GABAergic abnormalities: Abnormalities in glutamate and GABA signaling may help account for the negative and cognitive symptoms of schizophrenia[3][6][11]. Dysregulation of these systems and changes in synaptic plasticity and neurodevelopment may affect the disorder's pathophysiology[11]. 3. Neuroanatomical changes: Neuroimaging and neuropathology studies have revealed reduced whole-brain volume, enlarged ventricles, decreased cortical gray matter, and abnormalities in specific regions like the prefrontal cortex, hippocampus, amygdala, and insula[3][4][11]. 4. Neurodevelopmental origins: Evidence from genetics and epidemiology suggests that, at least in some cases, the origins of schizophrenia lie in genetic and/or environmental disruption of early brain development[3][8]. 5. Synaptic dysfunction: Emerging evidence points to disturbances of synaptic function, possibly involving interneurons and abnormalities of neuronal connectivity[3][9]. 6. Immune and inflammatory processes: Neuroimmunological processes and neuroinflammation have been proposed as potential contributing factors[1][2]. In summary, schizophrenia appears to arise from complex interactions between multiple genetic vulnerabilities and environmental factors[10], leading to disturbances in neurotransmission, brain structure and function, and neural connectivity. Further research integrating findings from genetics, molecular biology, neuroimaging, and other domains is needed to fully elucidate the neurobiology of this disorder[5][7][10].