Relevant bibliographies by topics / Schizophrenia – Risk factors

Academic literature on the topic 'Schizophrenia – Risk factors'

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Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Schizophrenia – Risk factors"

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Pulver, Ann E., Kung-Yee Liang, C. Hendricks Brown, Paula Wolyniec, John McGrath, Lawrence Adler, Doreen Tam, William T. Carpenter, and Barton Childs. "Risk Factors in Schizophrenia." British Journal of Psychiatry 160, no. 1 (January 1992): 65–71. http://dx.doi.org/10.1192/bjp.160.1.65.

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The risk for schizophrenia among first-degree relatives of schizophrenic probands obtained from an epidemiological sample using family history methods was examined to determine whether month of birth of the proband was associated with familial risk. The results of this study of the first-degree relatives of 106 female schizophrenics and 275 male schizophrenics suggested that the relatives of probands born in the months February to May had the highest risk, although the association between month of birth and familial risk among the male probands was present only for those relatives who had onset of schizophrenia before the age of 30.
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Baron, Miron, and Rhoda Gruen. "Risk Factors in Schizophrenia." British Journal of Psychiatry 152, no. 4 (April 1988): 460–65. http://dx.doi.org/10.1192/bjp.152.4.460.

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The association between the familial risk for schizophrenia and season of birth was studied in 88 schizophrenic patients. An increased risk for schizophrenia and ‘spectrum’ disorders was demonstrated among the first-degree relatives of winter and spring-born schizophrenic patients. However, patients with a family history of schizophrenia and ‘spectrum’ disorders did not differ from patients with no family history with respect to season of birth. Season of birth was unrelated to the sex of the patient, birth order, age at onset, or clinical subtypes (paranoid vs non-paranoid, as defined by the RDC, and ‘narrow’ vs ‘broad’, as defined by Taylor & Abrams' 1975 criteria). The morbid-risk data support a ‘stress-diathesis' hypothesis whereby environmental factors (in this case a seasonally varying viral insult may be implicated) interact with genetic vulnerability to increase the risk for schizophrenia.
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Weyerer, Siegfried. "Social Risk Factors in Schizophrenia." Psychological Reports 74, no. 3 (June 1994): 795–800. http://dx.doi.org/10.2466/pr0.1994.74.3.795.

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In analyzing the relationship between social factors and schizophrenia one can distinguish two research strategies. Studies can focus on individual differences or the aggregate level. Several investigations indicate that social factors, e.g., low socioeconomic status, single status, ethnic group, are significantly associated with the prevalence of schizophrenia. To explain this relationship most investigators favor the hypothesis of social selection rather than a social causation. This view is also supported by an ecological study of the incidence of psychiatrically treated schizophrenic disorders in the city of Mannheim.
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Boydell, Jane. "Risk factors for schizophrenia." Expert Review of Neurotherapeutics 1, no. 2 (November 2001): 183–91. http://dx.doi.org/10.1586/14737175.1.2.183.

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Owen, Michael J., and Shôn W. Lewis. "Risk Factors in Schizophrenia." British Journal of Psychiatry 153, no. 3 (September 1988): 407. http://dx.doi.org/10.1192/bjp.153.3.407a.

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Sacchetti, E., A. Vita, G. M. Giobbio, M. Dieci, and C. L. Cazzullo. "Risk factors in schizophrenia." British Journal of Psychiatry 155, no. 2 (August 1989): 266–67. http://dx.doi.org/10.1192/bjp.155.2.266a.

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Hultman, Christina M., Arne Öhman, Sven Cnattingius, Ing-Marie Wieselgren, and Leif H. Lindström. "Prenatal and neonatal risk factors for schizophrenia." British Journal of Psychiatry 170, no. 2 (February 1997): 128–33. http://dx.doi.org/10.1192/bjp.170.2.128.

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BackgroundThe present study examines the effects of independent, single pre- and perinatal risk factors and rates of obstetric complications upon the subsequent development of schizophrenia.MethodThis study was based on prospectively recorded birth records of 107 cases (82 with schizophrenic disorders and 25 with other psychotic reactions) and 214 controls, individually matched by gender and time and place of birth. Variables univariately associated with significantly elevated risk were entered in a logistic regression model.ResultsA high non-optimality summary score (> or = 7 complications of 34 possible) was a significant risk estimate for the total index group (OR 4.58, 95% CI 1.74–12.03) and the 82 schizophrenic patients (OR 3.67, CI 1.30–10.36). Patients with 2–6 complications also had an increased, although lower, risk (OR 1.67, CI 1.02–2.75). A disproportionate birth weight for body length (OR 3.57, CI 1.77–7.19) and a small head circumference (OR 3.93, CI 1.32–11.71) were the strongest independent risk factors.ConclusionsA contribution of obstetric complications to the risk of schizophrenia was confirmed. Only aberrations in physical size remained as individual independent risk factors.
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Lyons, Michael J., Jonathan Huppert, Rosemary Toomey, Rebecca Harley, Jack Goldberg, Seth Eisen, William True, Stephen V. Faraone, and Ming T. Tsuang. "Lifetime prevalence of mood and anxiety disorders in twin pairs discordant for schizophrenia." Twin Research 3, no. 1 (February 1, 2000): 28–32. http://dx.doi.org/10.1375/twin.3.1.28.

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AbstractThere have been long questions about the relationship of schizophrenia to other mental disorders. Lifetime DSM-III-R diagnoses of mood and anxiety disorders in twins with clinically diagnosed schizophrenia (n = 24) and their non-affected co-twins (n = 24) were compared with twins from pairs without schizophrenia (n = 3327) using a sample from the Vietnam Era Twin Registry. Schizophrenic probands had significantly elevated rates of all included disorders (bipolar disorder, major depression, dysthymia, generalized anxiety disorder, panic disorder, and PTSD) compared with controls (P < 0.01). The odd ratios comparing co-twins of schizophrenic probands with controls was greater than three for every disorder, but did not attain statistical significance. A similar pattern was observed when analyses were restricted to only monozygotic twins (n = 12). Consistent with other studies, schizophrenics appeared to have higher rates of a range of mental disorders. Our results suggest that schizophrenia per se represents a risk factor for other psychiatric disorders, but the absence of significantly elevated risk among non-schizophrenic co-twins suggested that family environmental and/or genetic factors that contribute to risk of schizophrenia do not increase the risk of mood and anxiety disorders to the same extent that the risk of these other disorders is increased by the presence of schizophrenia. Twin Research (2000) 3, 28–32.
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Michie, Patricia T., Aaron Kent, Renee Stienstra, Rochelle Castine, Julie Johnston, Kellie Dedman, Helen Wichmann, et al. "Phenotypic Markers as Risk Factors in Schizophrenia: Neurocognitive Functions." Australian & New Zealand Journal of Psychiatry 34, no. 1_suppl (February 2000): A74—A85. http://dx.doi.org/10.1177/000486740003401s12.

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Objective To review the literature on neurocognitive measures as risk markers for schizophrenia and to present data from the Perth family study of schizophrenia. Of all the risk markers that have been identified, the most promising are deficits in sustained attention. Method Inclusion in the review was determined by whether the research addressed a number of key questions: methods of assessing sustained attention; evidence of sustained attention deficits in patients and first-degree relatives including children; the importance of attentional dysfunction in the schizophrenic process and functional outcome; and the biological basis of sustained attention deficits. Results Sustained attention deficits are evident in both patients and a proportion of their first-degree relatives, a finding replicated in preliminary data from the Perth family study. The literature suggests that the attention deficit is a stable enduring trait that is independent of clinical state. The neural basis of the deficit may be a functional disconnection between prefrontal and parietal cortex. Attention impairment is an important predictor of functional outcome in patients and the development of social dysfunction in adulthood in the at-risk offspring of patients. However, sustained attention deficits that are measured in childhood results in an unacceptable high false-positive rate (21%) when predicting which at-risk offspring of parents with schizophrenia will develop a schizophrenia spectrum disorder, although the overall classification accuracy (78%) is impressive. Conclusions The main findings are that sustained attention deficits are important risk markers for schizophrenia but need to be supplemented by other neurocognitive risk markers to improve predictive accuracy.
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Planas, P., R. Català, C. Madrid, S. Eduard, and S. Lira. "Metabolic Risk Factors in a Schizophrenic Community Sample (vallès Oriental, Catalonia, Spain)." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71418-x.

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Introduction:Life expectancy for individuals with schizophrenia is 20% lower than in general population. Medical illnesses, psychiatric comorbidities, less access to care, poverty and limited perception of illness are some of the most important factors associated with increased risk of morbidity. Cardiovascular death (CVD) is a major contributor to increased mortality in schizophrenia 2,3. Prevalence of obesity in patients with schizophrenia (40%-60%) is twice the rate of the general population (20%-30%). Obesity, high abdominal perimeter, serum lipid levels, and smoking are significant, Independent Risk Factors for CVD.Metabolic syndrome is a cluster of metabolic disturbances, which is associated with an increased risk of CVD.Objective:To estimate the prevalence of CVRF in schizophrenic outpatients treated at Granollers' CSM.Methods:Cross-sectional descriptive study about 100 schizophrenic outpatients treated at CSM Granollers. Data on sociodemographics, physical examinations, blood test parameters, CVRF history and treatments are recorded. Each CVRF is established according to international criteria and/or pharmacological treatment.Secondary objectives:•Prevalence of Metabolic Syndrome;•Antipsychotic drugs treatment.Variables - Sociodemographic data and Schizophrenia diagnosis:•Physical examination;•Lab parameters;•Other CV risk factors (smoking, alcohol intake…).Results and conlusions:Estimated prevalences for most of the CVRF in schizophrenic outpatients are, in general, higher than those expected of the same age group in the general population. Data presented can support therapeutic decision-making and suggests a need of new prevention and monitoring strategies. New guidelines for monitoring and intervention will be needed for monitoring and intervention.
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Dissertations / Theses on the topic "Schizophrenia – Risk factors"

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Lee, Heeyoung. "Protective and risk factors in adolescents with schizophrenia /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7263.

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Eriksson, Åsa. "Risk factors for criminal offending among men with schizophrenia." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-666-2/.

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Suvisaari, Jaana. "Incidence and risk factors of schizophrenia in Finland." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/kansa/vk/suvisaari/.

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Roberts, Seth. "Season of Birth and Risk for Schizophrenia." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1633.

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Background: Schizophrenia is a chronic, debilitating mental disorder characterized by positive (e.g., hallucinations, delusions) and negative (e.g., catatonia, flat affect) signs and symptoms. Many studies suggest that individuals born in winter or spring months are at increased risk for schizophrenia. Study Objectives: 1) To determine whether season of birth affects risk for schizophrenia in the Irish Study of High Density Schizophrenia Families (ISHDSF). 2) To examine, by computer simulation, power to detect genetic associations with schizophrenia under a variety of conditions and using different analytic strategies. 3) To test whether specific genes are associated with schizophrenia in the Irish Case Control Schizophrenia Study (ICCSS), using different analytic strategies to account for season of birth. Methods: A case-control design was used to examine the relationship between schizophrenia and season of birth. Cases were individuals from the ISHDSF diagnosed with schizophrenia. Controls were the general population of Ireland, with data provided by Ireland’s Central Statistics Office (CSO). The birth frequencies for each month or quarter were compared in the two groups by a chi square test. Computer simulations were conducted to examine power to detect schizophrenia susceptibility loci using either all cases or only cases born in high-risk months, under different conditions and models for how genetic risk and season of birth interact to influence risk for schizophrenia. Data for six genetic markers from the ICCSS were analyzed for evidence of association, using all cases, and then using only cases born in high-risk months. Setting and Study Participants: ISHDSF families were ascertained through inpatient psychiatric care facilities serving >95% of the Irish population. Diagnoses were established using DSM-III-R criteria, and birthdates were recorded for all individuals. The Irish CSO provided aggregate, population-level data for number of births in Ireland by month for the years 1976-2000 and by quarter for the years 1900-2000. The ICCSS is a sample of schizophrenic and control individuals who have been genotyped at many loci across the genome. Schizophrenics were ascertained through in- and outpatient psychiatric facilities, had diagnoses verified by an expert, and their birthdates recorded. Controls were selected from several sources, e.g. blood donation centers, and denied any lifetime history of schizophrenia. For each subject in the ICCSS, all four grandparents were born in Ireland or the United Kingdom. Results: Number of births in each month was compared for schizophrenics in the ISHDSF and general population controls, resulting in a chi square of 19.44 (p value ~ 0.054, 11 df). Simulations revealed that, in some circumstances, power to detect genetic associations was increased by restricting cases to those born in high-risk months. Analysis of data from the ICCSS revealed that restricting cases to high-risk birth months increased the evidence for association for three of six markers tested, two of which were associated with the gene FBXL21. Conclusions: Birth in the months of March, April, or May appears to be associated with elevated risk for schizophrenia in the ISHDSF. In attempting to find susceptibility loci for schizophrenia, restricting genetic association analyses to schizophrenics born in high-risk months may result in increased power to detect genetic association in some circumstances.
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Spencer, Michelle Kerry. "Examining the use of dynamic risk factors to predict high risk behaviours in people with schizophrenia." Thesis, University of Warwick, 2009. http://wrap.warwick.ac.uk/3261/.

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The following thesis discusses aspects of risk management within a dynamic framework. It focuses on risk management with people with schizophrenia, as they are considered to be at more risk than the general population both of harming others and harming themselves. The literature review summarises current research into suicide risk factors in the schizophrenia population. People with a diagnosis other than schizophrenia, such as schizoaffective disorder, are not included in the review. Studies that are dealing with factors that are open to change (dynamic), or that indicate or trigger imminent acute risk, are discussed. The literature is evaluated in terms of its methodologies, its findings and its place within a dynamic risk framework. Recommendations are made for future research. The main research paper explores a developing methodology to produce a high risk behaviour signature, utilising the concepts of early warning signs, psychosis relapse signatures, functional analysis and a dynamic risk model conceptualised from the sexual offending field. Support was found for staff’s ability to agree on relevance at a crude level for early warning signs of high risk behaviours compared to dummy signs, the occurrence of early warning signs, and the occurrence of high risk behaviour. Results are discussed further within the context of dynamic assessments of risk. The reflective review discusses philosophical, clinical and research reflections relating to the thesis. Three main themes are considered: the philosophical underpinnings of research; the impact of the process of research; clinical and ethical implications of research.
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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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Pukall, Monica G. "Postnatal risk factors in the etiology of schizophrenia : association with good premorbid adjustment." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30728.

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Research shows distinct premorbid subtypes in schizophrenia. While family history of schizophrenia and obstetric complications are associated with poor premorbid adjustment, risk factors associated with good premorbid adjustment, characterizing most patients, remain unidentified. Both childhood trauma and premorbid substance use appear to increase vulnerability to schizophrenia. The goals of this study were to determine the association among family history, obstetric complications, childhood trauma, and premorbid substance use; and secondly, to assess whether trauma and premorbid substance use are associated with good premorbid schizophrenia. Trauma and substance use were assessed in 26 schizophrenia patients whose mothers were asked about family history of schizophrenia and obstetric complications. Results suggest that childhood trauma may co-occur with a family history of schizophrenia; high premorbid cannabis consumption was significantly associated with an absence of family history. Childhood trauma and premorbid substance use, however, did not consistently predict a good premorbid adjustment profile.
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Davie, Brenda J. "Suicidality among individuals with schizophrenia, the interaction of personality and known risk factors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ30938.pdf.

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Pukall, Monica G. "Postnatal risk factors in the etiology of schizophrenia, association with good premorbid adjustment." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ64433.pdf.

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Thompson, Rhiannon. "Genetic and functional investigation of FXYD6 and MAP2K7 as risk factors in schizophrenia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4157/.

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Schizophrenia is a debilitating psychiatric disorder with a prevalence of around 1% worldwide. It is an extraordinarily complex syndrome, which encompasses multiple psychological domains leading to the impairment of a range of symptoms. These symptoms are categorised as positive symptoms, negative symptoms and cognitive deficits. The profile of cognitive deficits is broad and severe, and is likely to be present in most, if not all patients. Despite cognitive enhancement being recognised as an important treatment target in schizophrenia, the discovery of an effective treatment has been met with difficulty. The degree of psychosis is subject to numerous genetic and environmental factors. Family, twin and adoption studies show schizophrenia is unequivocally a genetic disorder, however the genetics behind schizophrenia are indisputably complex as it is not characterised by a single causative gene. A number of candidate genes have been implicated in schizophrenia. Recent genetic association studies have found an association for two genes, FXYD6 and MAP2K7, as risk factors in the susceptibility to schizophrenia. However the roles of these genes in the underlying mechanisms of the symptoms of schizophrenia are unknown. To address this I utilise two mouse models, one containing homozygous disruption of Fxyd6 (Fxyd6-/-) and one heterozygous for Map2k7 (Map2k7+/-). I employ a range of molecular and behavioural tests to investigate the roles FXYD6 and MAP2K7 in schizophrenia- like phenotypes in these mice. FXYD proteins are a family of seven single-span transmembrane proteins, all thought to be regulators of the Na+ K+ ATPase pump in a tissue-specific fashion. Up until now, FXYD6 function and its role in the risk to schizophrenia remain unclear. To address this I firstly investigated the association between FXYD6 and schizophrenia in a Northern European population using a genetic association study. However from this study I was unable to confirm an allelic or haplotypic association between FXYD6 and schizophrenia. Furthermore there was also no evidence for a role of epistatic interactions between FXYD6 and MAP2K7 in the risk of schizophrenia. A putative functional link for FXYD6 in schizophrenia was explored further using Fxyd6-/- mice. The in situ hybridisation technique was utilised to reveal the expression of Fxyd6 in the mouse brain. Fxyd6 is interestingly expressed in the prefrontal cortex and hippocampus, two brain regions associated with schizophrenia and learning and memory. In addition, I have shown for the first time that disruption of Fxyd6 results in a significant deficit in Na+ K+ ATPase activity in the forebrain, confirming that FXYD6 is a modulator of mouse brain Na+ K+ ATPase activity. Anxiety- like behaviours and hyperlocomotion were explored Fxyd6-/- mice. However activity in plus maze and open field tests, and response to amphetamine or ketamine was not altered in comparison to wildtype mice. Nonetheless subtle deficits observed in prepulse inhibition suggest potential deficits in neurotransmission in Fxyd6-/- mice may be present. Interestingly, Fxyd6-/- mice displayed deficits in working memory at delays of 5 seconds, indicating cognitive deficits. The molecular characterisation and insight into the phenotype of Fxyd6-/- mice are encouraging to investigate the role of FXYD6 in underlying mechanisms of schizophrenia-like symptoms further. MAP2K7 belongs to the family of Map Kinases which have key roles in the regulation of a diverse range of cellular processes such as gene expression, apoptosis and synaptic plasticity. The brain expression of Map2k7 was previously unknown, however this study utilised the in situ hybridisation technique to show expression in regions associated with schizophrenia, including the PFC and the hippocampus. For the reason that the homozygous disruption of Map2k7 is embryonically lethal, mice heterozygous for the disruption Map2k7 were used to explore the role of MAP2K7 in the susceptibility to schizophrenia. RTqPCR confirmed a modest but significant reduction of Map2k7 in these mice. The heterozygous deletion of Map2k7 results in alteration of glutamate receptor Grin1 expression, a receptor reported to have altered expression in schizophrenia. Furthermore, Map2k7+/- mice display cognitive deficits, as observed by increased perseverative responding in the working memory task. Despite not exhibiting deficits in PPI, social behaviours or neurochemical deficits in GABAergic markers, Map2k7+/- mice revealed altered sensitivity to amphetamine, suggesting alterations in dopaminergic circuitry. In conclusion, this study provides an insight in to the functional roles of FXYD6 and MAP2K7. Although the roles of FXYD6 and MAP2K7 as risk factors in schizophrenia still requires further elucidation, these results provide evidence of a putative role for both genes in some areas of the underlying neuronal activity associated with schizophrenia-associated symptoms. Furthermore, results from this study suggest both strains of mice are potential rodent models of cognitive impairments.
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Books on the topic "Schizophrenia – Risk factors"

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Häfner, Heinz, ed. Risk and Protective Factors in Schizophrenia. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7.

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Vulnerability to psychopathology: Risk across the lifespan. 2nd ed. New York: Guilford Press, 2010.

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Risk and protective factors in schizophrenia: Towards a conceptual model of the disease process. Darmstadt, Germnany: Steinkopff, 2002.

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McGorry, Patrick D., Alison Yung, and Lisa Phillips. Treating Schizophrenia in the Prodromal Phase. Informa Healthcare, 2004.

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Early Clinical Intervention and Prevention in Schizophrenia. Humana Press, 2003.

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PhD, Stone William S., Faraone Stephen V, and Tsuang Ming T. 1931-, eds. Early clinical intervention and prevention in schizophrenia. Totowa, N,J: Humana Press, 2004.

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Early clinical intervention and prevention in schizophrenia. Totowa, NJ: Humana Press, 2003.

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Brar, Jaspreet S. Epidemiology of Schizophrenia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199331505.003.0003.

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Epidemiology can help us understand who is at risk for developing a disorder, what may happen to them, and perhaps even why people get the disorder to begin with. In this chapter, we will review the incidence and prevalence of schizophrenia and related psychotic disorders, as well as factors affecting such rates. Risk factors for psychosis include socio-demographics (e.g., gender, age, migrant status, class), predisposing factors (e.g., season of birth, perinatal trauma), and precipitating factors (e.g., substance use, psychosocial stress). We will highlight controversial issues such as traumatic life events, prenatal infection, and cannabis use, considering how epidemiological factors can shed light on the pathogenesis of schizophrenia and related illnesses.
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A, Miller Gregory, ed. The behavioral high-risk paradigm in psychopathology. New York: Springer, 1995.

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Wolfram an der Heiden (Assistant), Franz Resch (Assistant), Johannes Schröder (Assistant), and Heinz Häfner (Editor), eds. Risk and protective factors in schizophrenia: Towards a conceptual model of the disease process. Steinkopff-Verlag Darmstadt, 2003.

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Book chapters on the topic "Schizophrenia – Risk factors"

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McGrath, John J., and Robin M. Murray. "Environmental Risk Factors for Schizophrenia." In Schizophrenia, 226–44. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327298.ch11.

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Gattaz, W. F., W. L. Abrahão, and R. Foccacia. "Environmental risk factors of psychosis." In Risk and Protective Factors in Schizophrenia, 133–38. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_12.

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Klosterkötter, J. "Predicting the onset of schizophrenia." In Risk and Protective Factors in Schizophrenia, 193–206. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_17.

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Häfner, H., K. Maurer, W. Löffler, W. an der Heiden, R. Könnecke, and M. Hambrecht. "The early course of schizophrenia." In Risk and Protective Factors in Schizophrenia, 207–28. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_18.

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Resch, F. "Discussion: protective interventions in schizophrenia." In Risk and Protective Factors in Schizophrenia, 321–23. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_27.

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Weiser, M., A. Reichenberg, J. Rabinowitz, H. Knobler, I. Grotto, D. Nahon, K. Soares-Weiser, and M. Davidson. "Risk factors for schizophrenia in adolescents." In Search for the Causes of Schizophrenia, 122–32. Heidelberg: Steinkopff, 2004. http://dx.doi.org/10.1007/978-3-7985-1953-4_8.

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Goldstein, Michael J. "Risk Factors and Prevention in Schizophrenia." In International Perspectives Series: Psychiatry, Psychology, and Neuroscience, 191–212. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3248-3_9.

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Maier, W., M. Rietschel, M. Linz, and P. Falkai. "Genetics of schizophrenia and related disorders." In Risk and Protective Factors in Schizophrenia, 9–28. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_2.

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Parnas, J., and J. W. Carter. "High-risk studies and neurodevelopmental hypothesis." In Risk and Protective Factors in Schizophrenia, 71–82. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_6.

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Harrison, G., and W. Eaton. "Migration and the social epidemiology of schizophrenia." In Risk and Protective Factors in Schizophrenia, 113–22. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_10.

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Conference papers on the topic "Schizophrenia – Risk factors"

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Ginanjar, Rizky, Alhadi Bustamam, and Hengki Tasman. "Implementation of regularized Markov clustering algorithm on protein interaction networks of schizophrenia's risk factor candidate genes." In 2016 International Conference on Advanced Computer Science and Information Systems (ICACSIS). IEEE, 2016. http://dx.doi.org/10.1109/icacsis.2016.7872726.

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Reports on the topic "Schizophrenia – Risk factors"

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Li, Mengdie, Yating Yang, Haixia Wang, and Tianhao Bao. Meta-analysis of risk factors for metabolic syndrome in schizophrenia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0023.

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Library, Spring. Schizophrenia & the Mental Fog. Spring Library, December 2020. http://dx.doi.org/10.47496/sl.blog.18.

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