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Abstract
Schizophrenia is deadly mental disorder that is seen in individuals during their early twenties. The disorder however has definitive cure and patients may experience symptoms for this disease throughout their lives. Many hypotheses have come out about the cause of the disease though none among them fully explains its pathophysiology. These hypotheses range from genetics to brain chemistry, structure and even environmental factors. Schizophrenia is presented by hallucinations, delusions, impaired cognitive activity, unorganized or abnormal motor movements and the inability to express emotions. Different researches have tried to explain some of these behaviors, how they come about and what medication can be the most appropriate. Schizophrenia having existed for decades, we believe that one day we shall come to understand the mystery behind it, in terms of the causes and the way it manifests.
Expository Essay on Schizophrenia
Introduction
Schizophrenia is a rare and severe mental disorder that is characterized with delusions and constant hallucinations. Schizophrenia accounts for approximately less than one percent of mental illnesses in the world. The onset of the disease has been found to be in the individual’s early twenties and these symptoms persist throughout the entire life of the individual despite the individual receiving medication. Over the years a lot of studies on the causes of the disease have been going on yet the real cause of this grave disease has not been found. However, with advancement in technology and intricate studies done it is thought that this mental disorder has a genetic basis and to some extent environmental factors. It is therefore thought disorders, brain chemistry, structural abnormalities and environmental factors are responsible for the manifestation of this disorder.
Although no specific genes have been found to cause schizophrenia, scientists have hypothesized that schizophrenia could be caused by certain genes which are inheritable. Through studies it has been established that there is a possibility of the other identical twin getting this deadly disease if present in either one of them. Also if a family member is schizophrenic or either of the parents, there is a possibility of other family members becoming schizophrenic.
According to Labrie et al. (2009), the gene for 5-HT1A, a receptor for serotonin, is significantly associated with schizophrenia. The study was the first to indicate a positive association of genes and schizophrenia among the Han population, and hence could be a better evidence of genes being involved in schizophrenia. The study involved eight hundred and forty-six normal individuals who were the controls and seven hundred and fifty-two schizophrenics. Five single nucleotide polymorphisms were genotyped in the genes for 5-HT1A and 5-HT2A. The result showed that one of the single nucleotide polymorphism was largely associated with schizophrenia. Studies have shown that low levels or deficiency of D-serine in an individual’s brain play a role in the pathophysiology of schizophrenia. D-serine, which is synthesized in brain cells by serine racemase, is a very important modulator of N-methyl-D-aspartate receptor. Abnormal functioning of N-methyl-D-aspartate receptor is therefore thought to have a direct implication in the pathophysiology of schizophrenia.
According to Papiol et al. (2011), a research was conducted on the effects of reduced levels of D-serine on mice which displayed some schizophrenic behaviors. Point mutations I genomes of the experimental mice was introduced by N-nitoso-N-ethylurea mutagenesis (ENU). This was to obtain serine recimase mutation in the mice. Western blot analysis using both monoclonal and polyclonal antibodies showed loss of serine recimase protein in the brain of these mice. The experimental mice were then interbred with the interbred with the control mice to get heterozygous mice. The mutant mice’s brain showed no or reduced levels of serine recimase protein. They also displayed schizophrenic behaviors like impaired prepulse inhibition, difficulties in sociability and spatial discrimination. Deficiency or low levels of D-serine affects N-methyl-D-aspartate receptor function and so results into reduced glutamic neurotransmission. N-methyl-D-aspartate receptors are special receptors that also act as ion channels found in nerve cells. These receptors are thought to be involved with synaptic plasticity which is a cellular mechanism involved in learning and memory. Synaptic plasticity is dependent on calcium ions influx through these receptors. Disruption in the function of these receptors as a result of reduced D-serine therefore results into schizophrenic behaviors (Symtheis, 2004). [“Write my essay for me?” Get help here.]
Research through DNA microarray studies has also linked oligodendrocyte dysfunction to schizophrenia. Oligondentric dysfunction basically refers to the down regulation of oligodentricite-related genes. According to Sujitha, et al. (2014), about a research done on abnormalities in myelination related genes, gene expression in oligondenrocytes and myelination was investigated in schizophrenia brains. In the experiment, fifteen brains from schizophrenic individuals and other fifteen normal individuals were used. Schizophrenia brains were used as experimental while the other brains were used as their controls. Quantative polymerase chain reactions and indexing-based differential polymerase reactions were used in screening the two sets of brains for differences in gene expression. Results from the experiment showed reduction in genes related to oligodentrocyte and myelin in the schizophrenia brains.
I t is, thus, hypothesized that disruption of axonal myelination by oligodentrocytes is what results to brain disconectivity and impaired cognitive functions. Myelination is essential for the rapid conduction of nerve impulses in nerve neurons. Oligodentritic down regulation therefore affects the process of myelination and therefore the process of nerve impulse transmission. Deficient nerve impulse transmission is the direct consequence of impaired neural, cognitive and glial functions as observed in schizophrenic patients.[Need an essay writing service? Find help here.]
One of the characteristic patients of schizophrenia is their inability to interpret or bring out emotions in tonal variations invoices and so find difficulties in social cognition. According to Kantrowitz et al. (2015), on Auditory Emotion Recognition Deficits, schizophrenics demonstrated difficulties in the recognition of the various emotions as depicted by the base pitch and pitch variability. In the experiment frequency modulation was used in creating base pitch modulations and pitch variability to mimic the tonal variations found in speech. These frequency modulations were to be used as the stimulus for different intended emotions. The experiment comprised of forty-three patients of schizophrenia and thirty-six controls who were subjected to this modulations. Mismatch negativity was also assessed in these patients. Majority of the patients in the experiment showed significant reductions in mismatch negativity across the frequency modulations. They also showed impairments in auditory emotion recognition and frequency modulation stimulus recognition.
Regions of the brain such as the amygdala, anterior insula, auditory cortex and the inferior frontal gyrus are thought to be involved in auditory emotional recognition. Abnormalities in the above regions of the brain lead to difficulties in recognition of emotions in speech which happens to be the case with schizophrenic patients (Roberts 2013).[Click Essay Writer to order your essay]
Conclusion
Schizophrenia for many decades has been a mystery to doctors and the public. People have always wanted to know the real cause of the disease, what those suffering the disease go through and why they behave in the given manner. Through research, scientists have been able to give some of these explanations. It is therefore thought that genetics, structural abnormalities in the brain and disorders in brain chemistry could be the main cause. These findings also try to explain why these patients present with the given symptoms. For instance impaired cognitive activity of the brain can be related to demyelination in the brain and oligodentric down regulation. However these findings are not enough and so the need for more research thanks to the ever developing technology.
References
Sujitha, S, P., Banerjee, M., Lakshmanan, S., Harshavaradhan, S, Gunasekaran, S and
Gopinathan, A. (2014). 5-Hydroxytryptamine (serotonin) 2A receptor gene polymorphism is associated with schizophrenia. Indian J Med Res, 140(6):736-43
Papiol, S., Begemann, M., Rosenberger, A., Friedrichs, H., Ribbe, K., Grube, S., Schwab, M.
H., Jahn, H., Gunkel, S., Benseler, F., Nave, K.-A. and Ehrenreich, H. (2011), A phenotype-based genetic association study reveals the contribution of neuregulin1 gene variants to age of onset and positive symptom severity in schizophrenia. Am. J. Med. Genet., 156: 340–345.
Kantrowitz, J,T., Hoptman, M,J., Leitman, D, I., Moreno-Ortega M., Lehrfeld, J,M., Dias E.,
Sehatpour, P., Laukka, P., Silipo, G & Javitt, D,C. (2015). Neural Substrates of Auditory Emotion Recognition Deficits in Schizophrenia. J NeoroSci, 35(44):14909-21.
Roberts, D. L., & Penn, D. L. (2013). Social cognition in schizophrenia: From evidence treatment. Oxford: Oxford University Press.Labrie, V., Fukumura, R., Rastogi, A., Fick L,J., Wang, W., Boutros, P,C., Kennedy, J,L.,
Semeralul, M,O., Lee F,H., Baker, G, B., Belsham, D, D., Barger, S,W., Gondo, Y., Wong, A,H. & Roder, J,C. (2009).Serine racemase is associated with schizophrenia susceptibility in humans and in a mouse model. Hum Mol Genet, 18(17):3227-43.
Smythies, J. R. (2004). Disorders of synaptic plasticity and schizophrenia. San Diego:
Elsevier/Academic Press.
