Schizophrenia is a complex and heterogeneous disease that affects over 1.5 million people in the United States alone. It causes structural abnormalities in multiple brain regions as well as alters neuronal signaling causing a plethora of symptoms that affect an individual’s day-to-day life. Globally it accounts for almost 1% of disability adjusted life years (DALYs), yet there is no known cure (Samele, 2007).
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However, for the disease to manifest it is currently thought that there must be both a genetic vulnerability, as well as environmental factors that result in a disease state. There is significant evidence showing that prenatal malnutrition (in specific regards to folate and vitamin D), childhood trauma, IQ and social cognition, social stressors, adolescent cannabis use, and expression of endogenous retroviruses all contribute to the development of schizophrenia (Davis, 2015). The large role epigenetics plays in the development schizophrenia presents an untapped potential to decrease rates of the disease through preventative treatment.
Schizophrenia is a form of psychosis that manifests in the early 20s for males and late 20s for females. While the exact mechanisms of the disease are unknown it is hypothesized that it results from improper neural development leads to the widespread dysfunction of multiple pathways in the brain. Functional scans show abnormal activity in both the frontal and temporal lobes as well as a reduction of tissue volume in these regions. This decrease in volume is thought to be a result of thinning of the cerebral cortex in the frontal and temporal lobes. Schizophrenic patients also typically have larger ventricles that control subjects. This is hypothesized to be the result of decreased tissue volume (Aleman, 2014). Increased dopamine secretion by the ventral tegmental area (VTA) is also commonly seen in schizophrenia; this causes abnormalities in the mesocorticolimbic pathway. This pathway is thought to be the main contributor to positive symptoms and the target for most anti-psychotic medications used to manage symptoms (Aleman, 2014).
The disease is characterized by 3 different subsets of symptoms: positive, negative, and cognitive. Positive symptoms are the most distinct symptoms of the disease and are categorized by an additional feature in which there is no corresponding normal phenotype. These symptoms include hallucinations, delusions, and catatonic behavior. Negative symptoms are the loss of normal function including the lost ability to express and distinguish emotions as well as loss of motivation. This is usually seen in the form of avolition (loss of interest/motivation), alogia (poverty of speech), and flat affect (inappropriate response). The third and final subset of symptoms are classified as cognitive and are generally more subtle. When tested schizophrenic patients often show decreased cognitive functioning, memory consolidation, and learning abilities- this relationship is linear, with more severe cases showing greater cognitive declines (Vacic,
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