Schizophrenia Problem essay

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Schizophrenia is a mental disorder, which distorts the personality of a person and makes it difficult for him/her to interact socially with other people. Schizophrenics usually are unable to distinguish between the real and unreal things, they are unable to think clearly, and have abnormal emotional responses to different events in life, cannot act normally in social situations (Kim, Ku, Lee, Choi & Kim, 2012). The causes of schizophrenia are not clear, and most of the models that have been proposed are still speculative. This essay explores possible biopsychological causes of this disease.

Many scientists have posited that schizophrenia develops as a result of a combination of genetic and environmental factors (Owen, O’Donovan, Thapar & Craddock, 2011). Genetic factors have been implicated for the malfunction of certain proteins that are vital to the normal function of the brain.

Risk genes are genes that have a large role to play in the development of plasticity during the development of brain circuits (Gilmore, 2010). The complexity of the human brain implies that the brain circuits are extremely intricate, and minor changes in the circuitry of the brain may lead to an improper way of responding to changes in the environment (Knapp & Parrish, 2011). For instance, some genes have been implicated for the increased activity of D-amino acid oxidase, which decreases the modulation effect of D-serine on the NMDA receptor, hence increasing susceptibility to schizophrenia. However, no conclusive evidence has come up to prove this model correct (Hadlich, Kirov, Lampinen & Zonneveld, 2010).

The treatment of schizophrenia should take into consideration the fact that genetic factors that cause it are correlated with environmental factors. Since schizophrenia seems to result from a problem in the synaptic connections in the brain, the treatment should consider boosting the function of certain receptors, such as the NMDA receptor. This could be achieved by inhibiting glycine transporters, so as to desaturate the vicinity of the NMDA receptor (Javitt, 2009). This could be a treatment to schizophrenia.

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