Schizophrenia is characterized by premorbid psychological deficits, onset of psychosis in late adolescence, and psychological deterioration in adulthood.! The pathophysiology of the disease involves both genes and environment.2 The etiology of the disease is attributed to the failure of normal neuronal development due to environmental factors (such as obstetric complications or maternal viral infections) or a genetic defect manifesting itself during gestation or the perinatal period. Such defects alter the development of the eNS in some way. The resulting developmental deficit accounts for the premorbid cognitive and psychosocial dysfunction in schizophrenia.3 The onset of psychotic symptoms in adolescence or early adulthood may be related to an excess in the normal synaptic pruning that occurs in certain brain regions, such as the prefrontal cortex.4 Specifically, psychological stress during this period can stimulate perturbations in neuronal activity that could otherwise be endured without long-term psychological consequences.5 The neurotransmitter alterations, including phasic and tonic dopamine transmission,6 serotonin receptor dysfunction,? and NMDA receptor hypofunction,8 can contribute to the positive, negative, and cognitive symptoms of schizophrenia that emerge during adolescence. In some schizophrenic patients, persistent, recurrent sensitization of the dopamine system over time9 or oxidative stress by glutamate induced neurotoxicity!O can lead to the neurodegeneration manifested by persistent morbidity, treatment resistance, and clinical deterioration. In this chapter, we describe the potential role of immunological mechanisms in the pathophysiology of schizophrenia, focusing on neurodevelopment, neurotransmitters, and neurodegeneration.
|Title of host publication||Neuropsychiatric Disorders and Infection|
|Number of pages||6|
|ISBN (Print)||1841845205, 9781841845203|
|Publication status||Published - 2005 Jan 1|
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