Biological Explanations for Schizophrenia

• The Genetic Basis of SCZ

  SCZ runs in families, though as they share the same environment and the same genes, the link has weak evidence. Though Gottesman's family study shows there is a strong relationship between the degree of genetic similarity and shared risk of SCZ. Identical twins- 48% risk, Children- 13% risk, Parents- 6% risk, Grandchildren- 5% risk.
• The Genetic Basis of SCZ- Candidate Genes

  Individual genes associated with risk of inheritance. Though there are a number of genes which provide a small increased risk, meaning SCZ is polygenic- requiring a number of genes to work in combination. Different studies have identified different candidate genes, meaning SCZ is also aetiologically heterogenous as different combinations lead to the condition.
• The Genetic Basis of SCZ- Candidate Genes

  Ripke et al carried out a large-scale study using data from genome-wide studies (looking at the full genome not just particular genes) of SCZ. Finding that there were 108 genetic variations that were associated with increased risk in a sample of 37,000. Genes associated included those linked to the functioning of neurotransmitters like dopamine.
• The Dopamine Hypothesis- Neurotransmitters

  Brains chemical messengers, they work differently in those with SCZ. Dopamine is widely believed to be involved; it is important in the functioning of several brain systems which may be implicated in SCZ symptoms.
• The Dopamine Hypothesis- Hyperdopaminergia in Subcortex

  Original DH focuses on the role of high levels or activity of dopamine in the subcortex (the central areas of the brain). For example, an excess of dopamine receptors in Broca's area (responsible for speech production) may be associated with speech poverty and/or auditory hallucinations.
• The Dopamine Hypothesis- Hypodopaminergia in Cortex

  Recent versions of the DH focus on abnormal dopamine systems in the brain's cortex. Goldman-Rakic et al identified that low dopamine levels in the prefrontal cortex (responsible for thinking and decision making) contributed to negative symptoms of SCZ. It may be that both hyper and hypo levels of dopamine are correct explanations, placed in different brain regions to explain SCZ.
• Neural Correlates of SCZ

  Measurements of the structure or function of the brain which correlate with experiences. With SCZ, both positive and negative symptoms have neural correlates.
• Neural Correlates of SCZ- Negative Symptoms

  Avolition: ventral striatum is believed to be involved in the anticipation of reward, contributing to our sense of motivation. Meaning abnormality of this area can be involved in the development of avolition. Juckel et al measured its activity levels in SCZ patients and found lower levels than observed controls. There is a negative correlation between activity and severity of overall negative symptoms.
• Neural Correlates of SCZ- Positive Symptoms

  Allen et al scanned brains of individuals experiencing auditory hallucinations and compared them to a control group whilst they had to identify if pre-recorded speech was theirs or others. Found there were lower activation levels in the superior temporal gyrus and anterior cingulate gyrus in hallucination group. Showing lower activity is a neural correlate for auditory hallucinations.
• AO3: Sources of Evidence for Genetic Susceptibility

  Adoption studies, like that of Tienari et al, clearly show that children of those with SCZ are at heightened risk even when adopted into families with no history of SCZ. There are studies, like Ripke et al, which look at risks at a molecular level which show particular genetic variations increase the risk. IDA- Nomothetic, Objective

  Though it may not be entirely genetic, there are a number of environmental factors which increase risk too.
• AO3: Mixed Evidence for Dopamine Hypothesis

  Support- dopamine agonists, like amphetamines, which increase levels of dopamine are found to make symptoms worse, and can produce SCZ-like symptoms in people undiagnosed- Curran et al. And Antipsychotic drugs work by reducing dopamine levels which help sufferers symptoms- implying dopamine is important.
• AO3: Mixed Evidence for Dopamine Hypothesis

  Support- Studies by Lindstroem et al show that chemicals needed to produce dopamine are taken up faster in the brains of people with SCZ, implying that they produce more dopamine.
• AO3: Mixed Evidence for Dopamine Hypothesis

  Opposing Evidence- Some genes identified by Ripke et al code for the production of other neurotransmitters, so although dopamine is one important factor, so are other neurotransmitters. Current research has looked at the effect of glutamate (Moghaddam and Javitt). Meaning dopamine isn't a complete explanation.
• AO3: Correlation-Causation Problem

  Though neural correlate studies alert researchers to the brain areas that aren't functioning correctly, this doesn't prove that the unusual activity caused the symptom. Though it may be abnormalities in the ventral striatum which cause avolition, or the symptoms themselves may mean less information passes through which reduces the overall activity. This is then a limited explanation, there may even be a third variable influencing them both.
• AO3: The Role of Mutation

  SCZ can take place without family history of it. One explanation for this is mutation of parental DNA- this can be caused by radiation, poison, or viral infection. Brown et al found a positive correlation with the paternal age (associated with increased risk of sperm mutation) and risk of SCZ. Increasing from 0.7% with fathers under 25, and to over 2% with fathers over 50.
• AO3: Role of the Psychological Environment is Important but Unclear

  Evidence supporting the role of biological factors is overwhelming. Though there is also evidence to suggest an important role for environmental factors, including psychological factors like family functioning during childhood. This is particularly evident as the probability of developing SCZ is less than 50% in MZ twins. Meaning SCZ isn't purely genetic.