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Relevant bibliographies by topics / Schizophrenia – Genetic aspects

Academic literature on the topic 'Schizophrenia – Genetic aspects'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "Schizophrenia – Genetic aspects"

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Morozova, A. Yu, E. A. Zubkov, Ya A. Zorkina, A. M. Reznik, G. P. Kostyuk, and V. P. Chekhonin. "Genetic aspects of schizophrenia." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 117, no. 6 (2017): 126. http://dx.doi.org/10.17116/jnevro201711761126-132.

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Karayiorgou, Maria. "Genetic aspects of schizophrenia." Clinical Neuroscience Research 1, no. 1-2 (January 2001): 158–63. http://dx.doi.org/10.1016/s1566-2772(00)00015-3.

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Böök, Jan A. "Genetic aspects of schizophrenia." Clinical Genetics 19, no. 5 (April 23, 2008): 357. http://dx.doi.org/10.1111/j.1399-0004.1981.tb00726.x.

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Bellivier, F. "Schizophrenia, antipsychotics and diabetes: Genetic aspects." European Psychiatry 20, S4 (December 2005): S335—S339. http://dx.doi.org/10.1016/s0924-9338(05)80187-7.

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AbstractThe relatively high comorbidity of type 2 diabetes and schizophrenia may suggest a shared biological susceptibility to these twoconditions. Family studies have demonstrated an increased risk of diabetes in unaffected relatives of patients with schizophrenia, consistent with a heritable susceptibility trait. Linkage analyses have identified several loci that are associated with schizophrenia and some of these, notably those on chromosomes 2p22.1-p13.2 and 6g21-824.1 have also been observed in linkage studies in type 2 diabetes. In addition, the dopamine D5 receptor on chromosome 5 and the tyrosine hydroxylase gene on chromosome 11 have both been suggested as candidate genes in schizophrenia and may also be implicated in susceptibility to poor glycaemic control. In addition, an increased rate of type II diabetes has been observed in some patients treated with antipsychotics. Potential neurochemical substrates of this effect include the histamine H1 receptor, the 5-HT2C serotonin receptor or the β3 adrenoreceptor. However, the search for a genetic basis to the association between diabetes and schizophrenia is still in its infancy, and much further work needs to be performed, including the systematic screening of all confirmed susceptibility loci and quantitative trait locus mapping of glycaemic control.

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Muir, Walter J. "Genetic aspects of the biology of schizophrenia." Current Opinion in Psychiatry 5, no. 1 (February 1992): 2–5. http://dx.doi.org/10.1097/00001504-199202000-00002.

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Trifu, Simona Corina, Anca Vlăduţi, and Antonia Ioana Trifu. "Genetic aspects in schizophrenia. Receptoral theories. Metabolic theories." Romanian Journal of Morphology and Embryology 61, no. 1 (2020): 25–32. http://dx.doi.org/10.47162/rjme.61.1.03.

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Kambarova, D. K., and A. G. Golubev. "Biochemical and genetic aspects of pathogenesis of schizophrenia." Journal of Evolutionary Biochemistry and Physiology 47, no. 5 (October 2011): 407–19. http://dx.doi.org/10.1134/s0022093011050021.

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Galderisi, S., and M. Maj. "Deficit schizophrenia: An overview of clinical, biological and treatment aspects." European Psychiatry 24, no. 8 (December 2009): 493–500. http://dx.doi.org/10.1016/j.eurpsy.2009.03.001.

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AbstractThe concept of deficit schizophrenia is regarded as one of the most promising attempts to reduce heterogeneity within schizophrenia. This paper summarizes the clinical, neurocognitive, brain imaging and electrophysiological correlates of this subtype of schizophrenia. Attempts to identify genetic and non-genetic risk factors are reviewed. Methodological limitations of studies supporting the efficacy of atypical antipsychotics in the treatment of the syndrome are highlighted. Two decades of research on deficit schizophrenia have failed to prove that it represents the extreme end of a severity continuum in schizophrenia, while some findings support the claim that it may be a separate disease entity.

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Popov, Nikolay T., Vili K. Stoyanova, Nadezhda P. Madzhirova, and Tihomir I. Vachev. "Epigenetic aspects in schizophrenia etiology and pathogenesis." Folia Medica 54, no. 2 (October 1, 2012): 12–16. http://dx.doi.org/10.2478/v10153-011-0082-x.

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ABSTRACT Epidemiological evidence suggests that etiology of schizophrenia may involve both the influence of genetic factors specific for the individual and the impact of the environment. It is quite likely that a crucial role in the disease development is played by molecular mechanisms mediating the interaction between genes and environment. Modern research have shown that epigenetic mechanisms or chemical modifications of deoxyribonucleic acids (DNA) and histone proteins remain unstable throughout life and can be changed by environmental factors. Thus the epigenetic mechanisms outline an attractive molecular hypothesis of the environment modelling role and the environmental contribution to schizophrenia progression. We give in the present study a general outline of schizophrenia as a pathological entity and discuss the role and involvement of environment versus genetic determinant (nature versus nurture) in the pathophysiolgical processes. Additionally, we focus on DNA methylation discussing the evidence for the role of that process in schizophrenia. Thirdly, we review the post-translational histone modifications and their role in schizophrenia. These investigations might surely lead further to the development of epigenetic therapy that looks promising in regard to symptom alleviation and the disease-associated cognitive deficit.

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Syvälahti, E. K. G. "Biological Factors in Schizophrenia Structural and Functional Aspects." British Journal of Psychiatry 164, S23 (April 1994): 9–14. http://dx.doi.org/10.1192/s0007125000292672.

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A number of factors have been proposed as being linked to schizophrenia: genetic, psychological, endocrinological, metabolic, environmental, virological, and auto-immunological factors, as well as neurotransmitter systems and structural disorders of the brain. All may act as predisposing, triggering, or functionally modulating factors in what is probably a condition composed of several types of disorder with varying aetiology. Neuroanatomical and neuromorphological data have revealed ventricular enlargement and diminished frontal and temporal lobe volume in some patients. These changes are concentrated particularly in the hippocampus/parahippocampal gyrus/amygdala, but are relatively small and span some overlap with healthy subjects. Twin studies suggest that at least some of these changes may result from other than genetic factors. Functional disturbances of the brain have also been connected with frontal and temporal structures in some schizophrenic patients. Of the single neurotransmitter substances, dopamine and serotonin appear to represent some of the central restitutive mechanisms whose function is to maintain mental stability; the understanding of their interplay with other neurotransmitters such as noradrenaline, acetylcholine, GABA, and glutamate, should provide a more integrated view of both normal and disturbed brain function.

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Dissertations / Theses on the topic "Schizophrenia – Genetic aspects"

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Zhang, Xiaowei, and 张晓薇. "Twin studies on childhood externalizing behavior and schizophrenia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208003.

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Wycoff, Jeffrey M. L. "Neuropsychological patterns in RISC identified schizotypic subjects." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/864928.

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The present study employed the Rust Inventory of Schizotypal Cognitions (RISC) to identify an experimental group of schizotypics (as well as an appropriate control group). It was hypothesized that these individuals would show patterns on a battery of neuropsychological tests (e.g., Category Test, Tactual Performance Test, and Trails B from the Halstead-Reitan Neuropsychological Battery; Expressive Speech, Memory, and Intellectual Processes Scales from the Luria-Nebraska Neuropsychological Batter; and the Rey Complex Figure Test) similar to those exhibited by actual schizophrenics. Findings indicated that schizotypes do show a pattern of deficits on neuropsychological tests similar to those observed in diagnosed schizophrenics. These results lend validity to the RISC as an instrument for use in selecting those at-risk for schizophrenia. They also illustrate a possible neuropsychological vulnerability marker for schizophrenia.
Department of Psychological Science

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Wong, Nai-kei, and 黃乃淇. "Expression of myelin-related genes in an immune-precipitated mouse model of schizophrenia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4378026X.

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Wong, Hoi-man Emily, and 黃凱敏. "Genome-wide association analyses on complex diseases: from single-nucleotide polymorphism to copy numbervariation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50534099.

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Complex diseases, unlike Mendialian diseases, are often characterized by genetic heterogeneity and multifactorial inheritance, involving defects in genes from the same or multiple alternative pathways. Many congenital diseases and psychiatric disorders are complex diseases, and incur heavy health care burden on the society. With the advancement in high-throughput genotyping technologies and the availability of the human single nucleotide polymorphism (SNP) catalogue, genome-wide association study (GWAS) has been widely used to investigate the genetic component of complex diseases. Copy number variations (CNV) can also be identified using the data from the same SNP array. Aiming to identify more disease susceptibility loci for complex diseases, separate GWAS using a case-control design were conducted on anorectal malformations (ARMs) and schizophrenia. ARMs are rare congenital diseases with heterogeneous phenotypes which could probably be explained by the genetic heterogeneity among patients, while schizophrenia is a common psychiatric disorder that is well known for its multigenic inheritance. The GWAS studies on ARM and schizophrenia included 4,369 (patients: N=363; controls: N=4,006) and 1,231 Han Chinese (patients: N=381; controls: N=850) respectively. The two studies were mainly focused on investigating the contribution of rare CNVs to the diseases, involving analyses on global CNV burden, rare CNV association, protein-protein interaction (PPI) network, pathway and chromosomal aberrations. The associations of SNPs with ARMs were also examined. Apart from elucidating the genetic components in these two diseases, a systematic analysis on four CNV detection programs (CNV partition, PennCNV, QuantiSNP and iPattern) was also undertaken. In the study of schizophrenia, a new approach in CNV filtering which was based on latent class analysis was adopted to gather information from multiple CNV prediction programs. The study of ARMs revealed 79 genes which were disrupted by CNVs in patients only. In particular, a de novo duplication of DKK4 (an antagonist of WNT signaling) was identified, and addition of Dkk4 protein was demonstrated to cause ARMs in mice. Another 10 genes uniquely disrupted in ARMs patients are also related to WNT signaling. Interestingly, this pathway was also significantly inferred by CNV in patients with schizophrenia. A different set of genes related to WNT signaling was disrupted in ARMs patients and patients with schizophrenia. WNT signaling is crucial for the development of multiple parts in the embryo. The contribution of different WNT signaling pathways at different development stages may vary. Apart from the WNT signaling pathway, other genes with biological relevance were also implicated in the two studies through gene-network and pathway analyses. The results from these two GWAS studies support our existing understanding of complex diseases that defects in various interacting genes could contribute to the same disease. In summary, the CNV results from the two studies have demonstrated the genetic heterogeneity nature of these two complex diseases. The findings also uncovered a set of putative disease candidate genes, which can be used as reference materials for future genetic research for ARMs and schizophrenia.
published_or_final_version
Psychiatry
Doctoral
Doctor of Philosophy

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Truter, Erika. "Genetic association analysis of polymorphisms in four cytochrome P450 genes, the MDR1 gene and treatment-outcome in Xhosa schizophrenia patients." Thesis, Link to online version, 2007. http://hdl.handle.net/10019/350.

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Wright, Galen Egan Buckley. "Molecular genetic analysis of two genes, CYP2D6 and COMT, in the schizophrenia-susceptibility locus on chromosome 22q in the Xhosa population." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20366.

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Wolff, Anne-Lise. "A kinematic investigation of oculomotor and skeletomotor performance in schizotypy /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85104.

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Although heritability estimates of schizophrenia are high, studies attempting to identify specific genes for schizophrenia have been only modestly successful. Strategies to improve the power of genetic studies include the creation of homogeneous subtypes of schizophrenia based on symptom presentation, and the identification of behavioural abnormalities that reflect the presence of genes for schizophrenia ("behavioural markers of risk") even in the absence of the full clinical disorder. Oculomotor abnormalities are one of the most well-documented markers of risk. It is not known whether abnormalities in motor control are specific to the oculomotor system or whether they are found as well in other domains such as skeletomotor control. It is also not known whether different types of schizophrenia-related symptoms, which presumably have distinct neural bases, are associated with different behavioural abnormalities.
This thesis investigates oculomotor and skeletomotor function in clinically unaffected individuals who are at elevated risk for schizophrenia based on their scores on either a positive-symptom schizotypy questionnaire (Perceptual Aberration Scale) (n = 21) or a negative-symptom schizotypy questionnaire (Physical Anhedonia) (n = 20), and in Controls (n = 29).
In Manuscript 1, we review the evidence suggesting that skeletomotor deficits are present in neuroleptic-naive schizophrenia patients and high-risk populations. The review supports the notion of skeletomotor dysfunction in these groups and underscores the lack of studies using instrumentation to characterize the deficits. In Manuscript 2, we compare the oculomotor performance of positive-symptom and negative-symptom schizotypes to that of controls. Results suggest that smooth pursuit deficits identify high-risk individuals with either positive or negative symptomatology, while antisaccade deficits identify primarily individuals with positive symptoms. In Manuscript 3, we use high-speed instrumentation and kinematic measures to evaluate skeletomotor function, and to assess the relationship between oculomotor and skeletomotor deficits in positive and negative-symptom schizotypes. This study revealed differential patterns of skeletomotor deficits in positive- and negative-symptom schizotypy, with both patterns suggestive of frontal-striatal dysfunction. In general, oculomotor and skeletomotor deficits were not associated.
Together these results support the notion of motor deficits across domains in risk for schizophrenia. In addition, they highlight the importance of distinguishing between positive and negative symptomatology when investigating the pathophysiology of risk for schizophrenia.

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Morgan, Vera Anne. "Intellectual disability co-occurring with schizophrenia and other psychiatric illness : epidemiology, risk factors and outcome." University of Western Australia. School of Psychiatry and Clinical Neurosciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0209.

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(Truncated abstract) The aims of this thesis are: (i) To estimate the prevalence of psychiatric illness among persons with intellectual disability and, conversely, the prevalence of intellectual disability among persons with a psychiatric illness; (ii) To describe the disability and service utilisation profile of persons with conjoint disorder; (iii) To examine, in particular, intellectual disability co-occurring with schizophrenia; and (iv) To explore the role of hereditary and environmental (specifically obstetric) risk factors in the aetiology of (i) intellectual disability and (ii) intellectual disability co-occurring with psychiatric illness. This thesis has a special interest in the relationship between intellectual disability and schizophrenia. Where data and sample sizes permit, it explores that relationship at some depth and has included sections on the putative nature of the link between intellectual disability and schizophrenia in the introductory and discussion chapters. To realise its objectives, the thesis comprises a core study focusing on aims (i) (iii) and a supplementary study whose focus is aim (iv). It also draws on work from an ancillary study completed prior to the period of candidacy...This thesis found that, overall, 31.7% of persons with an intellectual disability had a psychiatric illness; 1.8% of persons with a psychiatric illness had an intellectual disability. The rate of schizophrenia, but not bipolar disorder or unipolar major depression, was greatly increased among cases of conjoint disorder: depending on birth cohort, 3.7-5.2% of individuals with intellectual disability had co-occurring schizophrenia. Down syndrome was much less prevalent among conjoint disorder cases despite being the most predominant cause of intellectual disability while pervasive developmental disorder was over-represented. Persons with conjoint disorder had a more severe clinical profile including higher mortality rates than those with a single disability. The supplementary study confirmed the findings in the core body of work with respect to the extent of conjoint disorder, its severity, and its relationship with pervasive development disorder and Down syndrome. Moreover, the supplementary study and the ancillary influenza study indicated a role for neurodevelopmental insults including obstetric complications in the adverse neuropsychiatric outcomes, with timing of the insult a potentially critical element in defining the specific outcome. The supplementary study also added new information on familiality in intellectual disability. It found that, in addition to parental intellectual disability status and exposure to labour and delivery complications at birth, parental psychiatric status was an independent predictor of intellectual disability in offspring as well as a predictor of conjoint disorder. In conclusion, the facility to collect and integrate records held by separate State administrative health jurisdictions, and to analyse them within the one database has had a marked impact on the capacity for this thesis to estimate the prevalence of conjoint disorder among intellectually disabled and psychiatric populations, and to understand more about its clinical manifestations and aetiological underpinnings.

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Hitzeroth, Angelika. "Association of genetic variants and the susceptibility to abnormal involuntary movements and tardive dyskinesia (TD) in Xhosa schizophrenia patients." Thesis, Stellenbosch : University of Stellenbosch, 2007. http://hdl.handle.net/10019.1/2147.

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Thesis (MSc (Genetics))—University of Stellenbosch, 2007.
No obvious explanations exist for the development of abnormal involuntary movements (AIM), but several hypotheses have been proposed for tardive dyskinesia (TD) development. Since TD seems to have a genetic basis, several genetic variants have been investigated in TD development in various populations. Few studies have focused on African populations. This study focused on genetic variants (previously investigated in other populations) and the development and severity of AIM and TD in a Xhosa schizophrenia population. Genotype and allele frequencies determined were compared to those described in the literature for other populations. Following a report of an association between Ala-9Val and schizophrenia in a Turkish population, this study subsequently investigated this association in the Xhosa population. MnSOD Ala-9Val was genotyped using HEX-SSCP analysis and the DRD3 Ser9Gly variant was genotyped using restriction enzyme digestion by MscI. Genotyping was followed by statistical comparisons of the various groups, as well as association analyses between the variant and schizophrenia (only for MnSOD), AIM, or TD development and severity. The groups included a Xhosa schizophrenia group, a subgroup of the Xhosa schizophrenia group that had AIM (AIM+) and did not have AIM (AIM-), a subgroup of the AIM+ group that had TD (TD+), and a healthy Xhosa control group. A possible interaction between Ala-9Val and Ser9Gly in the development of AIM and TD was also investigated. Lastly, it was attempted to genotype CYP2D6*4, CYP2D6*10 and CYP2D6*17 using various PCR methods followed by restriction enzyme analysis. MnSOD Ala-9Val genotype and allele frequencies were similar to those of the Turkish population, but differed to those of the Asian populations. No association between Ala-9Val and the development and severity of schizophrenia was found. However, a relationship between genotype and AIM or TD development was observed, as well as an association between TD severity and Ala- 9Val genotype. DRD3 Ser9Gly genotype and allele frequencies were similar to those of the African American population, but differed from other populations. No significant association between Ser9Gly and the development and severity of AIM or TD was detected, nor was an interactive effect between Ala-9Val and Ser9Gly in AIM or TD development observed. The genotyping of CYP2D6 proved difficult and these variants could therefore not be analysed. The CYP2D6*4 genotype and allele frequencies that could be determined from some samples, were similar to the frequencies described previously for African populations. While we did not find an association between Ser9Gly in TD or AIM development and severity, nor an interaction between Ala-9Val and Ser9Gly, we did observe a relationship between Ala-9Val and AIM or TD development and TD severity. The effect of this variant is probably small and other variants, specifically those in genes involved in free radical removal should be investigated in combination with Ala-9Val. With regard to CYP2D6 it is suggested that high-throughput genotyping methods (e.g. microarray technology) should be used in the future. This will enable simultaneous genotyping of several variants and can be used in various populations. This study is the first of its kind by focusing on the unique South African Xhosa population and TD or AIM development.

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Koen, Liezl. "Chromosomal aberrations in the Xhosa schizophrenia population." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/1189.

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Thesis (PhD (Psychiatry))--Stellenbosch University, 2008.
BACKGROUND: Schizophrenia is a heterogeneous illness resulting from complex gene-environment interplay. The majority of molecular genetic work done has involved Caucasian populations, with studies in these and Asian populations showing 2-32% of sufferers to have chromosomal aberrations. So far the discovery of a specific susceptibility mechanism or gene still eludes us, but the use of endophenotypes is advocated as a useful tool in this search. No cytogenetic studies of this nature have been reported in any African schizophrenia population. AIM: The aim of the study was to combine genotypic and phenotypic data, collected in a homogenous population in a structured manner, with the hope of characterising an endophenotype that could be used for more accurate identification of individuals with possible chromosomal abnormalities. METHODOLOGY: A structured clinical interview was conducted on 112 Xhosa schizophrenia patients. (Diagnostic Interview for Genetic Studies, including Schedules for the Assessment of Negative and Positive Symptoms.) Blood samples (karyotyping and/or FISH analysis) as well as urine samples (drug screening) were obtained and nine head and facial measurements were performed. Descriptive statistics were compiled with reference to demographic, clinical and morphological variables. Comparisons between mean differences for these variables were made.

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Books on the topic "Schizophrenia – Genetic aspects"

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Genetic models of schizophrenia. Amsterdam, Netherlands: Elsevier, 2009.

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Searching for the causes of schizophrenia. Oxford: Oxford University Press, 1994.

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Cortical deficits in schizophrenia: From genes to function. New York: Springer, 2008.

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Torrey, E. Fuller. Schizophrenia and manic-depressive disorder: The biological roots of mental illness as revealed by the landmark study of identical twins. New York: Basic Books, 1994.

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Dahlem Workshop on Biological Perspectives of Schizophrenia (1986 Berlin, Germany). Biological perspectives of schizophrenia: Report of the Dahlem Workshop on Biological Perspectives of Schizophrenia, Berlin 1986, October 26-31. Chichester: Wiley, 1987.

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Boklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self\soul, sex, and schizophrenia. Singapore: World Scientific, 2010.

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Hunter, Beatrice Trum, and Beatrice Trum Hunter. Gluten intolerance: The widespread genetic defect that can cause arthritis, enteritis, schizophrenia and other health problems. New Canaan, CT: Keats, 1987.

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Boklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self/soul sex, and schizophrenia. New Jersey: World Scientific, 2009.

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Boklage, Charles E. How new humans are made: Cells and embryos, twins and chimeras, left and right, mind/self/soul, sex, and schizophrenia. New Jersey: World Scientific, 2010.

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Lang, Mary V. Trends In Schizophrenia Research. Nova Biomedical Books, 2004.

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Book chapters on the topic "Schizophrenia – Genetic aspects"

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Scourfield, Jane, and Peter McGuffin. "Genetic aspects." In Schizophrenia in Children and Adolescents, 119–34. Cambridge University Press, 2000. http://dx.doi.org/10.1017/cbo9780511526800.007.

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Kinney, D. K. "Schizophrenia and Bipolar Disorder: Genetic Aspects." In International Encyclopedia of the Social & Behavioral Sciences, 13537–43. Elsevier, 2001. http://dx.doi.org/10.1016/b0-08-043076-7/03366-0.

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Kwon, Ester J., Takahiro Soda, and Li-Huei Tsai. "Neurodevelopment and Schizophrenia." In Neurobiology of Mental Illness, edited by Pamela Sklar, 327–37. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0025.

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A neurodevelopmental model of schizophrenia postulates that some of the key aspects of brain development that normally occur both pre- and post-natally are not occurring correctly, either in time or space. Complex neural circuitry needs to form and be modulated by experience. Classically, proliferation, migration, arborization and myelination occur prenatally. Elaboration and refining of dendritic trees and synapses as well as myelination of the nervous system continues through the first two-decade of life. There are opportunities for genetic and environmental abnormalities and variation to profoundly influence the trajectories of all of these critical functional processes.

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Brüne, Martin. "Schizophrenia spectrum and other psychotic disorders." In Textbook of Evolutionary Psychiatry and Psychosomatic Medicine, 159–76. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780198717942.003.0008.

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Schizophrenia spectrum disorders are characterized by the presence of delusions, hallucination, disorganized thinking, motor abnormalities, and/or negative symptoms. Behaviourally, schizophrenia patients have profound difficulties in regulating approach and avoidance, causing social withdrawal or aggressive behaviour. Evolutionary hypotheses of schizophrenia abound, but none covers all phenotypic aspects of the syndrome(s). Genetic risk for schizophrenia is partly conferred by genes that have undergone positive selection, whereby the reproductive advantage compensating for the reduced fecundity is as yet unknown. Environmental risk factors for schizophrenia comprise poverty, migration, and urbanicity, which has given rise to the hypothesis that individuals with schizophrenia are particularly sensitive to the exposure of strangers. In a more general vein, many signs and symptoms associated with schizophrenia can be interpreted from an evolutionary point of view. They pertain to diverse aspects of social life, including cooperation and trust (paranoia), mating (delusional jealousy, erotomania), and social rank (catatonic stupor, mutism).

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Andreasen, Nancy C. "The core dimensions of schizophrenia." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 565–73. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0057.

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Schizophrenia is a devastating illness that usually affects many aspects of a person’s life. The symptoms may be divided into two groups. ‘Positive’ symptoms include a variety of psychotic symptoms such as delusions and hallucinations. Although severe, they are less handicapping than negative symptoms such as avolition or anhedonia. Positive symptoms involve the presence of things that should be absent, while negative symptoms involve the absence of things that should be present. Dimensional approaches for classifying symptoms have also become popular in current nosology, proposing three dimensions: positive, negative, and disorganized. The course of the illness evolves over time; a prodrome is often present, followed by illness onset and a variable outcome. Good outcome predictors include good premorbid adjustment, high intelligence quotient, and good social relationships. The pathophysiology of the illness includes genetic, neuropathological, and neurodevelopmental components. A possible association with creativity may suggest reasons why the illness has persisted over many centuries.

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Jablensky, Assen, Hannah E. Jongsma, James B. Kirkbride, and Peter B. Jones. "Epidemiology of schizophrenia and related disorders." In Oxford Textbook of Neurologic and Neuropsychiatric Epidemiology, edited by Carol Brayne, Valery L. Feigin, Lenore J. Launer, and Giancarlo Logroscino, 277–92. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749493.003.0028.

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Epidemiological approaches to understanding the frequency, distribution, and determinants of psychotic disorders, such as schizophrenia, have played a vital role in delineating the aetiology and course of these conditions for almost a century. Despite several milestones, reviewed in this chapter, many methodological and clinical aspects of these disorders continue to provide challenges to studying the epidemiology of psychotic disorders, including issues of case definition, case ascertainment, and study design. After summarizing these challenges, we review the current neuropsychiatric epidemiologic knowledge of the incidence, prevalence, and aetiology of psychotic disorders. Here, we also provide a contemporary overview of the role that genetic, neurodevelopmental, demographic and environmental risk factors, including inflammation, traumatic life events, substance abuse, urban living, and minority status have on risk, course, and outcome of psychotic disorder. We conclude with future directions required to elucidate the interplay of these factors in contributing to the global burden of psychotic disorders.

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Large, Charles H. "Genetic association of voltage-gated ion channels with psychotic disorders." In Psychotic Disorders, edited by Michael A. P. Bloomfield and Oliver D. Howes, 335–40. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190653279.003.0037.

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A goal for the treatment of psychotic disorders, such as schizophrenia and bipolar disorder, is to correct the function of neural circuits that have been implicated in the range of symptoms from altered sensory perception to impaired cognition. However, this goal is complicated by the absence of an obvious lesion, genetic mutation, or even a clear disease process. The brains of people with psychotic illness just appear to work differently. Dopamine receptor blocking strategies repress the more florid symptoms of psychosis, but appear to do little to influence the underlying dysfunction of brain circuits, and they do not improve the patient’s cognition. Voltage-gated ion channels (VGICs) are proteins that define neurons: they are required for all aspects of neural processing and signaling. Could modulation of these highly dynamic proteins be useful in the treatment of psychosis? This chapter reviews examples of VGICs that have been linked to psychosis and that may take us toward the goal of better treatments for these devastating disorders. This chapter covers specific examples of chloride, calcium, potassium and VGIC channel pathology associated with psychosis.

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Tsuang, Ming T., William S. Stone, and Stephen V. Faraone. "Schizoaffective and schizotypal disorders." In New Oxford Textbook of Psychiatry, 595–602. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0080.

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This chapter focuses on two disorders in the schizophrenia ‘spectrum’: schizoaffective disorder and schizotypal personality disorder. The emphasis includes the clinical features, classification, diagnosis, epidemiology, aetiology, course, prognosis, and possibilities for prevention for each disorder. Some aspects will be underscored to reflect controversial issues, such as the heterogeneity apparent in each condition. Such issues relate to the accurate classification of the disorders, which is important for at least two reasons. First, it is essential to develop reliable and valid diagnostic criteria in order to study the aetiology of the disorders and then utilize that knowledge to develop rational and testable intervention strategies. Heterogeneity adds variance to the process that reduces both the reliability of diagnosis and also the statistical power of experimental designs to detect intervention/treatment effects. Second, the development of newer generations of psychopharmacological treatments holds the promise of matching more appropriate and efficacious medications with specific syndromes or types of symptoms. This trend underscores the importance of differential diagnosis in determining what treatment a patient will receive. Heterogeneity within a diagnostic category complicates achievement of this goal. Another area to be emphasized involves the goal of early interventions, in addition to palliative treatments for these disorders. In contrast, other areas such as the genetic aetiology of schizoaffective disorder and schizotypal personality disorder, and treatments for schizoaffective disorder, will receive less emphasis here, to avoid redundancies with other chapters in this volume. Each disorder will be considered separately, starting with a review of schizoaffective disorder, the more severe of the two spectrum conditions.

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Ghaemi, S. Nassir. "Fundamentals of Neurobiology." In Clinical Psychopharmacology, edited by S. Nassir Ghaemi, 17–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199995486.003.0002.

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This chapter examines the basic pharmacology of psychotropic drugs. Besides knowing what drugs do to certain chemicals or proteins in the brain, it is important to know where drugs affect those chemicals or proteins. There is some basic knowledge about neuroanatomy that is relevant to the clinical practice of psychopharmacology. It is accepted that neurobiology is an important factor in the etiology and pathophysiology of major psychiatric conditions—like schizophrenia and manic-depressive disease, as well as in other psychiatric clinical pictures. The general summary usually provided is that neurobiology represents a diathesis to psychiatric conditions, which is supplemented by environmental stress to produce observed clinical pictures. This mixture of genetics and environment is oversimplified in the minds of most mental health professionals. In fact, the mix depends on the illness. The biochemical neuroanatomy of the monoamines, glutamate, and GABA in the brain are discussed. Pharmacokinetic aspects of psychopharmacology are reviewed, including hepatic metabolism, drug half-lives, dosing, and tolerance and sensitization.

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