PubMed · 14855012
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1951-04-07. HYPOTHALAMUS.. https://pubmed.ncbi.nlm.nih.gov/14855012/
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A great number of studies show biological alterations in patients with schizophrenia, but many of these data are conflicting. Schizophrenia is a vastly heterogeneous disorder, most likely not caused by one etiological factor, but rather due to a complex network of different, interacting pathogenic influences. Variable clinical pictures may reflect different etiological factors. In a comprehensive theory of the origin of schizophrenic disorders, genetic and environmental influences cause changes in neuronal development which result in functional alterations of different neurotransmitter systems. Immunological research in schizophrenia was initially based on the "infection hypothesis" which was triggered by observing schizophrenia-like psychoses after influenza pandemic. Numerous immunological studies focusing on antibodies against specific viruses, unspecific antibodies and different other immune-phenomena were carried out in schizophrenia patients. Although the variability of the results from these studies is strikingly high, subgroups of patients with schizophrenia show an activated inflammatory response system with increased levels of proinflammatory cytokines and acute phase proteins. Furthermore, some investigations find changing activities in the T-cell system with a shift of TH-1 to an increased TH-2 activity. Endocrinological factors which may play a relevant role in the etiopathogenesis of schizophrenia include sex hormones and all changes caused by stress or other influences which are directly related to the HPA-axis. Alterations of the immune and the endocrinological systems might be caused by environmental factors like infections or exogenous stress. Due to the intensive interaction between the central nervous system, the immune system and different hormones the "development of a pathology" like schizophrenia can be seen in an integrative but multifactorial fashion. The clinical manifestation, the severity and the course of the disease might then be modulated by genetic vulnerability, the time of the "primary insult" -- which could be an infection, or psychological stress -- and its neuronal localisation and intensity. Different compensatory and decompensatory mechanisms in later life very likely play a crucial role for the further course of the disorder.
The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.
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