Academic consensus regarding the etiology of most mental disorders is quite difficult to achieve due to polygenic effects underlying the majority of mental disorders, complex gene-environment interactions, and the constant emergence of both supportive and contradictory evidence. Such complexity is natural to the study of most disorders; however, there are still some such as Schizophrenia that pose even more difficulty compared to others. Schizophrenia is a psychiatric condition that is marked by various psychotic symptoms that cause fluctuations in cognitive ability and impose distorted experiences onto the patient (Pinel, 2011). The aforementioned symptoms are grouped into positive and negative symptoms (Pinel, 2011). Positive symptoms of
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Furthermore, the two neurotransmitters that have been studied most in relation to Schizophrenia are dopamine and glutamate, which have yielded the Dopamine Hypothesis and Glutamate Hypothesis of Schizophrenia (Howes et al., 2015). Both of the aforementioned hypotheses attempt to trace Schizophrenic symptoms to a fluctuation in neurotransmitter activity in the brain. The updated version of the Dopamine Hypothesis states that schizophrenic symptoms are due to low levels of dopamine in frontal brain regions, and high levels of dopamine in the striatal regions (Lau et al., 2013). Furthermore, the updated Glutamate Hypothesis explains schizophrenic symptoms as the result of the malfunctioning of NMDA—n-methyl-d-aspartate—receptors (Howes et al., 2015). Lastly, evidence in support of these two hypotheses needs to be examined against contradictory evidence, which will allow for better understanding of the validity of each hypothesis. Moreover, this examination will help to determine if one hypothesis is more supported than the other, or if a departure from dichotomy and a combination of the two hypotheses yields a more accurate
Furthermore, the two neurotransmitters that have been studied most in relation to Schizophrenia are dopamine and glutamate, which have yielded the Dopamine Hypothesis and Glutamate Hypothesis of Schizophrenia (Howes et al., 2015). Both of the aforementioned hypotheses attempt to trace Schizophrenic symptoms to a fluctuation in neurotransmitter activity in the brain. The updated version of the Dopamine Hypothesis states that schizophrenic symptoms are due to low levels of dopamine in frontal brain regions, and high levels of dopamine in the striatal regions (Lau et al., 2013). Furthermore, the updated Glutamate Hypothesis explains schizophrenic symptoms as the result of the malfunctioning of NMDA—n-methyl-d-aspartate—receptors (Howes et al., 2015). Lastly, evidence in support of these two hypotheses needs to be examined against contradictory evidence, which will allow for better understanding of the validity of each hypothesis. Moreover, this examination will help to determine if one hypothesis is more supported than the other, or if a departure from dichotomy and a combination of the two hypotheses yields a more accurate