Intro
Schizophrenia is a disorder of abnormal cognition wherein oddities in perception, thinking, attention, learning, memory, manner relating to and others, congregate to form one of the most severe psychological illnesses in existence (Butcher, 2010).
Occurring in about 1% of the world’s population, schizophrenia is similarly prevalent across all cultures and ethnicities (Cunningham & Peters, 2014), and consists of several subtypes depending on the symptomology expressed (e.g. paranoid, disorganized, schizoaffective, catatonic).
The symptomology of the disease is subdivided into either positive or negative classifications. Positive symptoms implicated in the disease include delusion, hallucination, disorganized speech or clang associations,
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This is evident when we consider the subtypes and indeed individual cases of the illness deviate massively in their presentation, responsiveness to treatment and illness trajectory (Moore, Kelleher & Corvin, 2011).
An abundance of research into the cause of the disorder suggests that a combination of predispositional physiological factors and a multitude of environmental risk factors result in brain pathways developing abnormally.
Schizophrenia is a polygenic disease and thus cannot be explained by one mutated gene. Eyles, Feldon & Meyer (2012) have identified 40 genes implicated in the development of the disease, signifying that it is a cocktail within a certain genotype that confers susceptibility to the illness.
A study by Tinari et al. (2004) found that the genotype for higher risk in the illness only resulted in schizophrenia when an individual grew up in a dysfunctional vs. heathy family, suggesting that while biology provides the tinder, environment produces the spark.
Recent research by Trinity College’s Covin et al. (2014) suggests that mutations to genes that control epigenetic regulation (crucial to how brain develop and respond to experience) may cause