Role of Genes and Environment in the Aetiology of Schizophre

Role of Genes and Environment in the Aetiology of Schizophre INTRODUCTION Schizophrenia (schiz = splitting; phrene = mind) is generally characterized as the fragmentation of psychic functions (Bleuler, 1950) of which the absolute causes are unknown. It is defined and diagnosed based on Schneider (1959)’s ‘first rank symptoms’ which can be further categorized into positive (e.g. hallucination, delusion, etc.) and negative (e.g. avolition, catatonia, etc.), depending on the described and observed experiences of patients (Andreasen Olsen, 1982). This essay aims to review a wide range of scientific literature and research which attempted to study the influence of various genetic and environmental factors in the aetiology of schizophrenia based on the general assumption that this mental illness is a multifactorial disease and can be viewed as an outcome of gene-environmental interaction (Van Os, Rutten, Poulton, 2008). A case study on the effect of Cannabis use on schizophrenia (Caspi et al., 2005) is analysed in order to justify the signi ficance of gene-environment interaction. GENETIC FACTORS The study of genes and how they contribute to the aetiology of schizophrenia have always been the topics of interest for neurobiologist. Multiple twins studies have shown that identical twins of 100% shared genes carry almost 40 times higher risk than completely unrelated people in developing such mental disorder if one of them was schizophrenic (Kallman, 1946; Cardno et al., 1999). In fact, schizophrenia is a polygenic illness as no single significant schizophrenia gene has been identified and numerous candidate genes such as Dystrobrevin-binding protein 1 (dysbindin), neuregulin 1 (NRG1), Catechol-O-methyltransferase protein (COMT), and Disrupted-in Schizophrenia 1 (DISC1) are the aetiological factors (Ross et al., 2006). This essay intends to discuss the role of COMT with respect to the ‘dopamine hypothesis’ and dysbindin corresponding to the ‘glutamate hypothesis’. Two neurochemical models have evolved to become important theories accounting for the aetiology of schizophrenia. The dominant one is the ‘dopamine hypothesis’ which pinpointed the association of hyperfunction of dopamine system, critically at D2 receptors, with schizophrenia (Carlsson, 1988) but it is being challenged (Egan et al., 2001) and will be discussed in next section. Another recent model will be the ‘glutamate hypofunction hypothesis’ which suggested that N-methyl-D-aspartate (NMDA) receptors dysfunction and deficiency in glutamate production can lead to negative symptoms of schizophrenia (Olney, 1999; Coyle, 2006). ‘Dopamine hypothesis’ challenged: Introduction of inverted â€Å"U† model for COMT as the regulator of dopaminergic transmission COMT gene, being located at chromosome 22q11.2, is involved in the synthesis of dopamine metabolic enzyme and it regulates the dopaminergic transmission across synapses in the prefrontal cortex (Craddock et al., 2006; Tunbridge et al., 2006). Microdeletion of this chromosomal region resulted in Velo-cardio-facial syndrome (VCFS) and approximately one third of the patients suffering from VCFS were diagnosed to be with schizophrenia (Murphy et al., 1999), depictingthe significance of COMT in aetiology of schizophrenia via regulation of the release of dopamine transmitters in PFC. Two alleles, valine (Val) and methione (Met), found on COMT are involved in the functional polymorphism which alters the activity of dopamine metabolic enzyme. The relatively lower stability of the Met allele resulted in the lower enzyme activity, which in turn reduced dopamine breakdown and increased the concentration of dopaminergic transmission in the synapses. Consequently, individuals with Met-Met genotype were expected to be more susceptible to schizophrenia (Ross et al., 2006). In contrast, research has challenged the ‘dopamine hypothesis’ by demonstrating that both the patients with schizophrenia and individuals that inherited two copies of Val alleles (with decreased prefrontal dopamine level) exhibited the lowest PFC efficiency (Egan et al., 2001). This leads to the introduction of an inverted â€Å"U† model (see Figure 1) which illustrates the relationship between COMT genotype, PFC dopamine levels and prefrontal activity (Cools DEsposito, 2011). Glutamate hypothesis: Dysbindin as the regulator of glutamatergic transmission Dysbindin gene, being located at chromosome 6p22.3, was identified to have strong association with schizophrenia (Straub et al., 2002). There is a wide colocalisation of this gene with dystrobreyin in both presynaptic and postsynaptic regions of brain such as hippocampus (Benson et al., 2001). The level of dysbindin expression in the hippocampus and prefrontal cortex (PFC) of schizophrenia patients is consistently found to be significantly reduced (Talbot et al. 2004, Bray et al., 2005; Weickert et al, 2008). As a result of knockdown of endogenous dysbindin protein in culture by siRNA, a small interfering RNA, glutamatergic neurotransmission can be reduced. (Numakawa et al., 2004; Talbot et al., 2004). Besides, the reduced expression also significantly suppresses the synaptic transmission of glutamate in Drosophila’s brain (Shao et al., 2011) and reduces the excitation of NMDA as well as the expression of NR1 mRNA in the PFC of mice (Karlsgodt et al., 2011). These findings wel l supported the ‘glutamate hypothesis’ of schizophrenia, which proposed this mental disorder as an outcome of dysfunction of NMDA receptors and glutamatergic transmission. Limitations Although microdeletion of chromosome 22q11.2 increases vulnerability to schizophrenia, it is important to note that there might be other genes on the same location that can account for such illness as COMT is not the only gene in this location. Moreover, in contrast to the glutamate hypothesis’, reduced dysbindin expression in the hippocampus of mice increases NMDA-mediated current and long-term potentiation and increase glutamatergic transmission (Tang et al., 2009). This suggests that ‘glutamate hypothesis’ might not be applicable to the role of dysbindin in all brain areas. ENVIRONMENTAL FACTORS Studies using the approach of Magnetic Resonance Imaging (MRI) have consistently discovered significant brain abnormalities in schizophrenics such as reduced frontal lobes and cerebral cortex (Andreasen et al., 1986) which affected cognitive abilities. Reduced frontal cortex was later shown to have no correlation with familial influence but with environmental factors (Owen et al., 2012). Although Touloupoulou et al. (2010)’s study has demonstrated that genetic factors can explain the correlation between cognition and schizophrenia, the research also suggested that environmental factors can account for the weak link between them. This essay will then discuss the influence of prenatal and postnatal risk factors as well as childhood trauma in the aetiology of schizophrenia. Prenatal and postnatal risk factors in aetiology of brain abnormalities A meta-analysis has demonstrated the strong correlation between schizophrenia and prenatal or obstetric complications such as below standard birth weight, premature birth and perinatal hypoxic brain damage (Cannon, Jones Murray, 2002). During prenatal stage, deficiency in micronutrients such as folate, iron and vitamin D can interrupt physical development of fetus and result in low birth weight (Brown Susser, 2008). Maternal exposure to infectious pathogens such as herpes simplex virus type-2, rubella, polio etc. can also impact neurodevelopment in fetus and raise the vulnerability of offspring towards schizophrenia. Furthermore, hynoxia (deficiency in oxygen level) during perinatal stage significantly influences the development of gray matter which in turn induces schizophrenia (Opler et al., 2013). Childhood trauma and experiences in aetiology of abnormal functional and structural brain development Positive symptoms of schizophrenia such as hallucination is of strong association with undesirable childhood experiences such as abuse and neglect. Childhood trauma acts as a stressor which adversely alters the dopamine production system in hippocampus. Accordingly, the accumulated effect of abuse can trigger dysregulation of dopaminergic transmission as well as the onset of schizophrenia (Read, Os, Morrison Ross, 2005). The abnormal dopamine level (either too high or too low) is linked with the aetiology of schizophrenia, corresponding to the inverted ‘U’ model (Cools DEsposito, 2011). In addition, childhood abuse can lead to traumatic brain injury (TBI) which results in neurodegeneration and significant volume loss in various brain regions and eventually leads to the onset of psychosis (Keightley, 2014). 1316 GENE-ENVIRONMENT INTERACTION Case Study: COMT genotypes moderates the effect of adolescent cannabis-use on risk of schizophrenia in adulthood Strong evidences have signified the use of cannabis in adolescence as the modest risk factors for schizophrenia. Early use of cannabis is capable of increasing the risk of brain abnormalities and schizophrenia because the brains of adolescents are still under development and brain maturation is extremely susceptible to the deleterious effect cannabis use (Ehrenreich et al 1999; Pistis et al 2004; Pope et al 2003; Schneider and Koch 2003). Nonetheless, this environmental factor alone cannot be regarded as an aetiology of such mental disorder because a vast majority of the cannabis adolescent users do not exhibit schizophrenic disorders in adulthood (Caspi et al., 2005). Hence, the vulnerability of individuals towards adolescent-onset use of cannabis suggests a gene-environment interaction. In fact, COMT gene, as discussed above, is involved in regulating such trait. Individuals who have two copies of Val alleles carry the highest risk of schizophrenia at age 26 if cannabis abuse was f ound in their early stages, followed by Met-Val genotypes and adolescents who inherited Met-Met COMT genotype are least vulnerable to the abuse use of cannabis (Caspi et al., 2005). Thus, this clearly demonstrates the moderation effect of COMT on cannabis use and the gene-environment interaction. CONCLUSION In conclusion, understanding the role of various genes such as COMT and dysbindin in regulating the neurotransmission can help developing adequate medications which effectively tackle the mental illness. Identifying the influence of prenatal and obstetric complications as well as childhood experiences in aetiology of schizophrenia can also effectively prevent the onset of schizophrenia. Last but not least, studying the gene-environment interaction in the case of cannabis use reveals the multifactorial properties and intricate aetiology of schizophrenia. Hence, future research is encouraged to work on such interaction in order to pinpoint the main causes of such mental disorder. REFERENCES Andreasen, N. C., Olsen, S. (1982). Negative v positive schizophrenia: definition and validation.Archives of General Psychiatry,39(7), 789. Bleuler, E. (1950). Dementia praecox or the group of schizophrenias. Oxford/England: International Universities Press. 548. Carlsson, A. (1988). The current status of the dopamine hypothesis of schizophrenia. Neuropsychopharmacology. Cardno AG, Marshall EJ, Coid B, Macdonald AM, Ribchester TR, Davies NJ, et al. (1999). Heritability estimates for psychotic disorders.Arch Gen Psychiatry,56 (162), 8. Kallmann, F. J. (1946). The genetic theory of schizophrenia: an analysis of 691 schizophrenic twin index families.American Journal of Psychiatry,103(3), 309-322. Kety, S. S. R. D., Rosenthal, D., Wender, P. H., Schulsinger, F., Jacobsen, B. (1974). Mental illness in the biological and adoptive families of adopted individuals who have become schizophrenic: A preliminary report based upon interviews with the relatives.Journal of Psychiatric Research,10(2), 154. Ingraham, L. J., Wender, P. H., Kety, S. S. (1991). Characterization of genetically transmitted schizophrenia in Danish adoptees.Schizophrenia Research,4(3), 279-280. Ross, C. A., Margolis, R. L., Reading, S. A., Pletnikov, M., Coyle, J. T. (2006). Neurobiology of schizophrenia.Neuron,52(1), 139-153. Straub, R. E., Jiang, Y., MacLean, C. J., Ma, Y., Webb, B. T., Myakishev, M. V., Kendler, K. S. (2002). Genetic variation in the 6p22. 3 Gene DTNBP1 the human ortholog of the mouse dysbindin gene is associated with schizophrenia.The American Journal of Human Genetics, 71(2), 337-348. Shao, L., Shuai, Y., Wang, J., Feng, S., Lu, B., Li, Z., Zhong, Y. (2011). Schizophrenia susceptibility gene dysbindin regulates glutamatergic and dopaminergic functions via distinctive mechanisms in Drosophila.Proceedings of the National Academy of Sciences,108(46), 18831-18836. Olney, J. W., Newcomer, J. W., Farber, N. B. (1999). NMDA receptor hypofunction model of schizophrenia.Journal of psychiatric research,33(6), 523-533. Coyle, J. T. (2006). Glutamate and schizophrenia: beyond the dopamine hypothesis.Cellular and molecular neurobiology,26(4-6), 363-382. Talbot, K., Eidem, W. L., Tinsley, C. L., Benson, M. A., Thompson, E. W., Smith, R. J., Arnold, S. E. (2004). Dysbindin-1 is reduced in intrinsic, glutamatergic terminals of the hippocampal formation in schizophrenia. The Journal of clinical investigation, 113(9), 1353-1363. Weickert, C. S., Rothmond, D. A., Hyde, T. M., Kleinman, J. E., Straub, R. E. (2008). Reduced DTNBP1 (dysbindin-1) mRNA in the hippocampal formation of schizophrenia patients. Schizophrenia research, 98(1), 105-110. Karlsgodt, K. H., Robleto, K., Trantham-Davidson, H., Jairl, C., Cannon, T. D., Lavin, A., Jentsch, J. D. (2011). Reduced dysbindin expression mediates N-Methyl-D-Aspartate receptor hypofunction and impaired working memory performance. Biological psychiatry, 69(1), 28-34. Tang, T. T. T., Yang, F., Chen, B. S., Lu, Y., Ji, Y., Roche, K. W., Lu, B. (2009). Dysbindin regulates hippocampal LTP by controlling NMDA receptor surface expression. Proceedings of the National Academy of Sciences, 106(50), 21395-21400. Egan, M. F., Goldberg, T. E., Kolachana, B. S., Callicott, J. H., Mazzanti, C. M., Straub, R. E., Weinberger, D. R. (2001). Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia.Proceedings of the National Academy of Sciences,98(12), 6917-6922. Cools, R., DEsposito, M. (2011). Inverted-U–Shaped Dopamine actions on human working memory and cognitive control.Biological psychiatry,69(12), e113-e125. Opler, M., Charap, J., Greig, A., Stein, V., Polito, S., Malaspina, D. (2013). Environmental risk factors and schizophrenia.International Journal of Mental Health,42(1), 23-32. Gottesman, I. I., Bertelsen, A. (1989). Confirming unexpressed genotypes for schizophrenia: risks in the offspring of Fischers Danish identical and fraternal discordant twins.Archives of General Psychiatry,46(10), 867-872. Toulopoulou, T., Goldberg, T. E., Mesa, I. R., Picchioni, M., Rijsdijk, F., Stahl, D., Murray, R. M. (2010). Impaired intellect and memory: a missing link between genetic risk and schizophrenia?.Archives of general psychiatry,67(9), 905-913. Manoach, D. S. (2003). Prefrontal cortex dysfunction during working memory performance in schizophrenia: reconciling discrepant findings.Schizophrenia research,60(2), 285-298. Owens, S. F., Picchioni, M. M., Ettinger, U., McDonald, C., Walshe, M., Schmechtig, A., Toulopoulou, T. (2012). Prefrontal deviations in function but not volume are putative endophenotypes for schizophrenia.Brain, 138. Cannon, M., Jones, P. B., Murray, R. M. (2002). Obstetric complications and schizophrenia: historical and meta-analytic review.American Journal of Psychiatry,159(7), 1080-1092. Brown, A.S., Susser, E.S. (2008). Prenatal nutritional deficiency and risk of adult schizophrenia. Schizophrenia Bulletin, 34, 1054–1063 Read, J., Os, J. V., Morrison, A. P., Ross, C. A. (2005). Childhood trauma, psychosis and schizophrenia: a literature review with theoretical and clinical implications.Acta Psychiatrica Scandinavica,112(5), 330-350. Van Os, J., Rutten, B. P., Poulton, R. (2008). Gene-environment interactions in schizophrenia: review of epidemiological findings and future directions. Schizophrenia bulletin,34(6), 1066-1082. Caspi, A., Moffitt, T. E., Cannon, M., McClay, J., Murray, R., Harrington, H., Craig, I. W. (2005). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction.Biological psychiatry,57(10), 1117-1127. Keightley, M. L., Sinopoli, K. J., Davis, K. D., Mikulis, D. J., Wennberg, R., Tartaglia, M. C., Tator, C. H. (2014). Is there evidence for neurodegenerative change following traumatic brain injury in children and youth? A scoping review.Frontiers in human neuroscience,8. Schneider, K. (1959) Klinische Psychopathologie. New York/Stuttgart : Thieme Verlag.

NeoMed Tech

Subject line: Describe what went right and what went wrong with this venture. Add in how you would fix the Identified problems, If this was your company. Needed Technologies developed a diagnostic device used for cardiac testing, and is headquartered in Ohio. They developed a CAD screen system to detect coronary artery disease. The company was founded in 2000 and is based in Cleveland, Ohio.Needed Technologies was faced with a lot of difficult decisions at the beginning when it came to where their product would best fit and be most successful. They ad developed a technology that could fit Into many markets, but needed to choose a product path and market. Their continued challenges occurred due to the changes In the market direction of venture capital opportunities and the funding available, all due to changes in the economy at that time.Due to the lack of funding, and a continued decline in Venture Capital funding along with a downturn in the economy; I believe had the economic situa tion been different at the time when they needed venture capital funding, the would've faced less challenges. The management team and Board of Directors were selected carefully and all had the experience and the background needed for success In the product market space. Needed Technologies had a strong business plan, and had conducted extensive research in initial planning stages.I believe based on the reading materials in this chapter; they did all the right things in the planning and early development stages. Although Needed Technologies had to contend with big name competitors and major players in the diagnostic and imaging market such as GE Medical and Philips, also located in the Ohio region; their strategy to be headquartered in Ohio was a sound decision. However, they should've investigated further in the opportunity to obtain venture capital funding outside of the Ohio region.Perhaps they could've spent more time studying competitive business cases of companies Like competit or, Heartaches, who specializes In the BEST test. The Heartaches product, although more costly, had seen success and was widely accepted in the Medical field. Despite the added cost of the Heartaches BEST test, they were seeing success in the market. One strategy change I would've considered early on was not applying all resources of their technology into one area.Needed Technologies should've considered applying their initial product development to the technology of screening for drugs, drug delivery applications or detecting cancer. These areas would've possibly allowed for a quick to market product, without the additional approvals, quality standards applied in the medical equipment space, and FDA approvals needed. Bringing a simpler product to market first could've brought in revenue to fund the long-term reduce focus off CAD screen system.The profits from a drug screening or drug delivery product could've assisted in funding their long-term product focus, they missed an opportu nity to develop a quick revenue steam. Defense space, for detection of nuclear weapons, or dirty bombs. With the shift later in Venture Capital funding opportunities, they could've experienced success in this area as well. Bottom-line, they put all their eggs in one basket; they failed to have a backup product to develop a quick revenue stream to further fund their long-term goal.However, without a crystal ball that was a difficult decision. There were clear signs of shifts in investment opportunities, the shift indicted investments being shifted towards Homeland Security, military applications, and protection from various biological and chemical threats. Needed Technologies should shift some of their resources to developing a product to fit into that area, thus allowing them the opportunity to obtain additional venture capital funding, and perhaps developing a profitable product in the Homeland Security space.The revenue stream from this reduce would allow them later to proceed wit h their CAD screen system. There was another area of investment that should've been further investigated, â€Å"Angel Investors†, most of who are Entrepreneurs themselves currently, or at some point in their career. Inviting one of the Angel investors a seat on the board, as well as leveraging the experience they have gained from starting their own company, dealing with the challenges of starting a business, and investigating further Venture capital funding areas.Needed Technologies should've reached out farther than Just the Ohio-based Venture Capital firms, this would've allowed them a broader audience of investors and opportunity. I don't believe holding off for perfection is necessarily wrong, especially when dealing with, and factoring in the value of human life. The Needed Technologies board of directors and upper level management all appeared to encompass strong ethics and while that might be a weakness to others, ethics are important and should never be compromised. T oo many companies take the short cut to success and people get hurt.

Utilitarianism, Deontology and Virtue

Anthony B. FieldingUtilitarian, Deontological, and Virtue ethics The concept of utilitarianism is closely related to the philosophy of consequentialism. Basically this means that the moral and ethical value of a person’s action should be judged by the consequence of that action. Utilitarianism is believed to be the most important of the three ethical theories because it has helped shape our world’s politics, economics, and public policy. This ethical theory explains to us that we can determine the ethical significance by judging the consequence of that act.So basically I understand utilitarianism as; what is good for the majority is just and that happiness is the ultimate goal. An example of my own would be; the utilitarian would say that if six people were trapped on an island, two adult males and four small children with enough food to last two days if they all ate, but if the men did not eat, there would be enough for the children to eat for a week, it is ok for two men to starve to death if it meant that four children would live long enough to be rescued.Bound by our duties, walk the walk, and practice what you preach, the deontologist’s view of ethics. Contrary to utilitarianism, deontology says that there are some things that we should or should not do regardless of the consequence. Law enforcement officers wear a badge of honor ‘To serve and protect. ’ This motto is definitely one that describes deontology. Another popular slogan we hear is â€Å"Be all you can be. † This duty is demonstrated by our U. S. Army. A bodyguard’s duty is to protect his employer to the extent of endangering his own life.Virtue ethics questions how we should live our lives. A person is judged by his character and not by the actions he may uncommonly choose. Character building takes a lot of work. Character is introduced to us at a very young age by many sources, parents, grand-parents and teachers just to name a few. To me, virtue ethics can be confused as ‘do as I say and not as I do. ’ A person that practices virtue ethics may work for a company that sells automatic machine guns, but teach in his home that guns are bad.

Clothing And Identity And Social Class - 1342 Words

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There are ma ny ways in which people feel the need to express themselves through clothing such as: economic class, religious beliefs, social status and many more. The quote â€Å"Fashion provides one of the most ready means through which individuals can make expressive visual statements about their identities† (Bennet, 2005). Subculture groups allow people that share the same interests such as music, style and similar likes and dislikes into specific groups that they will fit into. One of the most important andShow MoreRelatedMen’s Clothing, and How Men Used Their Fashion and Appearance to Construct Their Masculine Identity, as Well as Their Social Class2137 Words   |  9 Pagesjackets, trousers, cravats, ties, and hats that provided plenty of material for asserting or maintaining social status (Delpierre, 1990). This essay focuses on men’s clothing, and how men used their fashion and appearance to construct their masculine identity, as well as their social class. 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