biological explanation of schizophrenia

• Family studies confirmed that risk increases in line with genetic similarity to a relative with the condition. Gottseman's (1991) large-scale family study shows that someone with an aunt with SZ has a 2% chance of developing it which increases to 9% if a sibling and 48% if they are an identical twin. The correlation represents both environment and genes as family members tend to share aspects of their environment yet this still gives strong support for the importance of genes 
• Early research looked for a single genetic variation in the belief 1 faulty gene could explain SZ. However, multiple genes appear to be involved and so SZ is polygenic. Ripke et al (2014) combined all previous data from genome-wide studies of SZ. The genetic make-up of 37,000 people with a diagnosis was compared to 113,000 controls. They found that 108 separate genetic variations that were associated with a slightly increased risk
• It can also have a genetic origin in the absence of a family history of the disorder. One explanation for this is mutation in the parental DNA, due to radiation, poison or viral infection. Evidence comes from positive correlations between paternal age, which is associated with increased risk of sperm mutation, and risk of SZ. 0.7% with fathers under 25 to over 2% in fathers over 50
• Neural correlates are patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience
• The ventral striatum is involved in reward processing and motivation, playing a key role in the brain's reward system as it is associated with pleasure. Research suggests dysfunction in this area is linked to negative symptoms, such as avolition. This is because the individual no longer experiences the same pleasure they normally would in situations which causes them to not participate in these due to reduced emotional connection and motivation. Juckel et al (2006) conducted fMRI scans and found lower activity in this area in individuals with the condition compared to healthy controls and also found that the lower the activity, the worse the severity of symptoms. This supports the idea that neural dysfunction in the area contributes to a lack of motivation
• the superior temporal gyrus is involved in auditory processing and language comprehension. Research suggests abnormalities in this region are linked to auditory hallucinations. Allen et al (2007) used fMRI scans to compare brain activity in individuals with the condition who experience auditory hallucinations and a control group. They found reduced activity in this area in those experiencing hallucinations
• The original dopamine hypothesis was based on the discovery that drugs used to treat the condition caused symptoms similar to those in people with Parkinsons, which is associated with low dopamine levels. Therefore, SZ may be the result of high dopamine levels in subcortical areas of the brain. An excess of dopamine receptors in pathways from the subcortex to Broca's area may explain specific symptoms such as speech poverty and auditory hallucinations
• Davis et al (1991) proposed the addition of the cortical hypodopaminergia such as abnormally low dopamine in the brain's cortex. Low dopamine in the prefrontal cortex which is responsible for thinking can explain cognitive problems such as negative symptoms