Biological Contributors of Mental Disorder Schizophrenia - Literature review Example

Biological Contributors of Mental Illness/Disorder – Schizophrenia Literature review There are various disorders that can lead to problems in mental health such as is Schizophrenia. Schizophrenia is a mental disorder which affects emotion, the person’s thinking and perception and his/her own behavior such that it will have impact on the individual, family and the society. People with Schizophrenia often have a different perception and loss contacts with the reality. The schizophrenia disorder usually appears at early adulthood, but it can appear later. It rarely affects young children and early teens (Van & Kapu, 2009; Mason & Miller, 2011). Finding the schizophrenia genes has proven to be elusive (Mason & Miller, 2011). Two theories have been used to find the gene for schizophrenia: one of them which are based on hypothesis uses neurobiology phenotypes and the other one free from hypothesis uses clinical diagnosis as phenotypes in its analysis. Due to the complexity of the condition, it is more proper to use both biological and clinical phenotypes to explain the complexity of schizophrenia. An inclusive use of intermediate phenotypes would be adopted to provide information about the schizophrenia genetics. There are different implications for the current study of schizophrenia. First, the biological aspect of the schizophrenia can provide a better knowledge and utilization of therapy techniques and principles in understanding and treatment of this condition. The identification of various factors in schizophrenia etiology is used by clinicians in its management. Secondly, the understanding of how particular brain systems contribute to schizophrenia symptoms will result in innovative cognitive treatment intervention. The gap between psychology and biological practitioners and researchers can also be bridged through better communication by sharing of information, concepts and principles. In addition, analysis of various aspects of the condition, which include social, psychological, neurological issues and others, may result in a better understanding of the complexity of the illness. The origin of schizophrenia has been debated over the years, with different causes being suggested and modified or rejected. Several studies suggest that the contributing factors to the disorder include the genetics, environment, social and psychological factors, gestation and prenatal development. There are five major types of schizophrenia that have been identified. They include: disorganized, paranoid, residual, catatonic and undifferentiated (Tsuang, 2011). Recent research into the occurrence and development of the disorder is neurodevelopmental based, which is based on the assumption that the disorder is a syndrome (Davi, 2002; Lashley, 2005; Berntson, & Cacioppo, 2009). However, its diagnosis is based on symptoms because neural correlation does not provide significant identification technique. This makes the research into the causes of schizophrenia highly fragmented (Berntson, & Cacioppo, 2009). Most researchers believe that schizophrenia results from a combination of genes (which can be inherited or acquired and makes the brain to be vulnerable) and the environment (Keshavan, 2008). However, there is no gene that causes the disorder which has been identified. Most researchers are based on how stress and vulnerability interact to develop and maintain the disorder. The disorder can develop at any age, most occurrence happens at or after teenage, with more prevalence on men than women (Halter, 2014). A study by Sprong (2008) shows that the disorder has strong genetic and transmissible characteristics and the people with first degree family members such as siblings with the disorder has 10% chances to develop the illness, compared to 1% chances for the general public (Sprong, 2008). However, the development of schizophrenia is inclined to the inherent features, but not determined by it. Although this conditions activates the disorder in many people, more than 55% of the people with no family relatives with symptoms of schizophrenia. The fact that people who can be influenced by the biological conditions do not develop the disorder shows that the biological contributions are not conclusive (Mason & Miller, 2011) Generally, the condition destroys the mental performance and is often characterized by constant hallucination and illusion. The disorder affects 1 percent of the people and especially the early phase of maturity like teenage (Moscou and Snipe, 2012). The neurobiology behind schizophrenia has not been known in spite of extensive research over the years. This may be due to heterogenic conditions in many cases. In etiological condition, genetics and environmental issues like prenatal, postnatal and gestation period plays a significant role in development of schizophrenia (Fenichel, 2005). The pharmaceutical treatment of schizophrenia has targeted a number of neurophysiologic processes. Several models of pathophysiology of nerophysiological processes which produces schizophrenia symptoms have been suggested (Moscou and Snipe, 2012). The models are based on various findings of neurotransmitters and brain region analysis. The study of neurophysiology of schizophrenia is complicated by different sets of clinical symptoms leading to a conclusion that the condition is as a result of a group of disorder, of which each have a their own pathophysiology and etiology. But no one has been able to describe what each of the set of disorders could be. Psychological symptoms which are specific and more reliable as the disorder marking and test for cognitive functions like memory, and attention is yet to be studied (Beck, 2011). In spite of the complexity of the disorder, biological explanation provide a better understanding of the whole complex schizophrenia process from genetic, gestation and prenatal etiological factors that would produce development changes (Beck, 2011). The genetic explanation of schizophrenia A human trait is determined by a pair of alleles which are inherited from the parents. Each of the alleles has got a potential to express themselves in humans, but can either be dominant or recessive. Dominant alleles suppress the traits of the recessive alleles, and the recessive alleles can express its traits when two recessive alleles pair up (Pennington 2000). Single-nucleotide polymorphisms (SNPs) are alterations which occur in the gene during the development of new cells, but can influence the formation of new cells within the central nervous system (CNS). This process has a potential to influence the genetic development of schizophrenia like neuroatanamic alterations, immune response, dopamine dysregulation, cognitive changes, cortisol sensitivity, etc (Pennington 2000). Torrey (1992) studied comprehensively about the potential of biological influence on the person’s vulnerability to the development of the disorder. He said that genes can be recessive or dominant and can either be polygenic or monogenic. He mentioned that genes can cause the development of the condition at any stage of development of schizophrenia, either by producing the schizophrenia symptoms directly through coding for dopamine dyregulation or indirectly by controlling the factors which influence the cognitive development. They may also influence the susceptibility to infection by virus. The idea that various genes have certain effects on the development of schizophrenia instead of a single genes being the only cause of the disorder has been sustain by other scholars. (Tsuanget al. 2001). Van & Kapu (2009) mentioned that neurochemical imaging research dopamine analysis of schizophrenia shows that the schizophrenia acute psychotic state is related to an increase in dopamine synthesis, release and synaptic dopamine resting state. This provides a link to the pharmaceutical treatment for the disorder (Van & Kapu, 2009). The causes of Schizophrenia have been debated by various scholars. Research has suggested that the environment, genetics, gestation, prenatal, social and psychological processes contribute to the development of the condition. Most of the studies suggest that the most cases of the occurrence of the schizophrenia are related to heredity. The studies include family, twin and adoption studies, including the association and genetic association studies (Gottesman & Wolfgram, 1991; Ingraham & Kety, 2000; Sullivan et al., 2003; Ban, 2004). Stevenson et al (2008) studied the nucleotide polymorphisms from various genome wide data. They found out that there was significant relationship between the risk of the schizophrenia illness and the alleles at several loci. They found out that the immunity and disease infections are related to alleles at certain loci. They also found that the results were consistent with the previous studies about schizophrenia (Stevenson et al., 2008). However, the identification of the specific genes which is responsible for development of the disorder has not been simple (Alberts et al., 2008). A study found out that around 80% of schizophrenia is associated with genetic and environmental factors (Van & Kapu, 2009). The genetic factors which are vulnerable to the influence by the environment may also affect twin heritage. Meta-analysis also shows that the schizophrenia is associated to paternal age of 40 and above, which indicates that the genetic mechanism plays a role. The common challenge is to relate these disciplines which may be required in the analysis of the models based on the interaction between the genes and the environment (Van & Kapu, 2009). Kinney et al. (2010) mentioned that an exposure to the unfavorable environment during gestation period may interrupt normal prenatal coding of the genes responsible for immunity. Thus create predisposing conditions in the immunity of an individual, making someone more vulnerable to infection or dysregulation of the immune system which are related to the CNS. They argued that the dormant vulnerability state in immunity is not normally revealed up to puberty, when the main modifications in the immunity systems begins, and partially due to the reduction in volume of the thymus gland. When the vulnerability emerges, the individual becomes vulnerable to the disease infections which lead to the onset of the disease (Kinney et al., 2010). This trend explains why the disorder normally occurs after puberty, after the volume of the thematic structure decrease to about one-fifth of the volume before puberty. The researchers also argued that various genetic and environment processes increases the risk of developing the schizophrenia are related to the increase in the vulnerability to the infectious disease and immunity disorders. Evidence relating to the genetic factors which influence of immunity in the development of the disorder was provided by Lencz et al. (2007). They discovered that the alleles in pseudo-autosomal section of XY chromosomes are more related to schizophrenia. They discovered that there are various lines of confirmations from different trials which indicated that the risk of developing the condition rises with the presence of alleles for two genes in the pseudo-autosomal region. The genes causes the alteration of the receptors structure of provocative cytokines and there expressions. They also mentioned that the effects of the cytokines will lead to the periodic changes of schizophrenia. The interleukin3, granulocyte-macrophage colony stimulating factor and cytokines are used in repair of CNS and in the modification of the neurotransmitters acetylcholine and GABA (Lencz et al., 2007). However, they didn’t confirm whether the association between the alleles at the cytokines receptor loci and the schizophrenia confirm the role of immunity response to the patophysiological infection or abnormal alterations (Kinney et al., 2010). White matter pathology With the introduction of sophisticated techniques such as the use of neuropathological, neuroimaging and electrophysiological methods, more advances have been made in the study of the relationship between schizophrenia and the brain structure. A meta-analysis shows that relatives at risk have regional and global brain decrease in volume with reference to the controls. Twins study on schizophrenia discordant show partial overlapping and genetic, including deficits in gray matter in heteromodal cortex (Cannon et al., 2002). Similar studies on close relatives reveal reduction in volume in some parts of the brain including thalami and in pre frontal lope volume (Pantelis et al., 2003; Job et al., 2007; Keshavan, 2008). This means that during early transition stages to psychosis, there is an active disease process in the genetic risk cases (Keshavan, 2008). Other studies reported the reduction in the structures of white matter like corpuscallosum and fiber tracts (Arnone et al., 2008). The changes in white matter relates to cognitive losses (Keshavan, 2008). The influence of white matter pathology on the schizophrenia is yet to be studied. The neural association studies can be done using diffusion tensor imaging or DTI. The technique tests the water diffusion gradient in the tissues like axons. Other methods include fractional anisotropy which shows the integrity of white matter. Studies on DTI revealed that fractional anisotropy in reduced in the white matter tracts for schizophrenia, such as unicinate fascilulus and corpus callosum (Keshavan, 2008). However, DTI has been shown to be insensitive to integrity of myelin (Kubicki et al., 2005). New technologies like magnetic transfer imaging, which measures changes in magnetic nuclei and water protons as it change from one chemical or physical state to the another, has been shown to produce better myelin reliability (Winterer and Konrad, 2008). The pathology of white matter is one of the main etiological discoveries in schizophrenia and is in agreement with cognitive deficiencies seen in the disorder; which is consistent with glutamatergic study of the disorder, as glutamatergic process plays role in integrity of glial (Kubicki et al., 2005; Haroutunian et al., 2007). The pathology of white matter is one of the main etiological discoveries on schizophrenia, which is also consistent to cognitive deficiency and dissociation thinking about the illness. The neural disconnectivity may be linked to the expression of dysregulated myelin gene, and the defects in the normal structure of myelin sheaths. Also Neuregulin gene has been report to important in the development of oligodendrocyte in schizophrenia individuals (Keshavan et al., 2008) In summary, there are various genetic and environmental factors which are related to the risk of developing schizophrenia. The factors are associated with the increase in the vulnerability and exposure of disease infections and immune infections especially those which are linked to the schizophrenia. The recent evidence of global alterations in the brain structure, reduction in volume of the brain volume regions including the connectivity such as those relating to prefrontal and medial cortices appears to give more conclusive causes of schizophrenia. Various researches on the biology behind schizophrenia are based on brain structure, neurochemical alteration and functionality in the different parts of the brain and their connectivity. These alterations seemed to be instigated early and continual to evolve in the course of the development of the illness, thus showing progressive sequential development of the derailment process. More modal and procedural difficulties remain. There is a need to apply accumulative knowledge in neurobiological studies in the study of schizophrenia so as to achieve better diagnosis. More critical etiological studies in needed. Reference Arnone, D., McIntosh, A. M., Tan, G. M., & Ebmeier, K. P. (January 01, 2008). Meta-analysis of magnetic resonance imaging studies of the corpus callosum in schizophrenia. Schizophrenia Research, 101, 1-3. Ban, T. A. (January 01, 2004). Neuropsychopharmacology and the genetics of schizophrenia: a history of the diagnosis of schizophrenia. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 28, 5, 753-62. Beck, A. T. (2011). Schizophrenia: Cognitive theory, research, and therapy. New York: Guilford Press. Berntson, G. G., & Cacioppo, J. T. (2009). 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