Biological explanations

• Evidence has shown that SZ runs in families.

  This evidence comes from a study done by Gottesman (1991) which shows that concordance rate in MZ twins was 48% or 0.48 compared to DZ twins of 17% or 0.17 compared to the general population of 1%.

  This shows that the influence of genes as both MZ and DZ share a similar environment and the MZ twins has a much higher concordance rate.
• Genetic studies have also revealed the influence of certain candidate genes. A study by Ripke (2014) studied the whole genome and compared 37,000 patients with SZ compared to 13,300 without it. It was found that 108 different genetic variations were associated with an increased risk associated with SZ.
• Dopamine hypothesis

  • dopamine is a chemical substance (neurotransmitter) manufactured in the brain that transmits messages between neurons (brain cells).
  • Dopamine appears to work differently in patients with S.
  • dopamine is particularly important in the functioning of several brain systems that may cause symptoms of SZ - in particular the cortex and subcortex.
• • Hyperdopaminergia = excessive levels of dopamine in the subcortex & Broca’s area = poverty of speech and auditory hallucinations
  • hypodopaminergia = low levels of dopamine in the prefrontal cortex which is responsible for decision making - negative symptoms
  • however current research has found that it might be over activity in some areas and low activity in other that are involved in SZ.
• Neural correlates

  Neural correlates look at the measurements of the structure and function of the brain that correlate with an experience, in this case SZ. Both positive and negative symptoms have neural correlates.
• Neural correlations = patterns of structure or activity in the brain that occur with a schizophrenic experience. As they occur simultaneously this could lead us to believe that the patterns observed are implicated in causing SZ.
• Avolition which involves motivation, has been associated with one of the main reward centres in the brain. The Ventral Striatum is crucial in the anticipation of reward. Juckel (2006) measured activity levels here and found lower levels of activity in SZs compared to controls.
• Positive symptoms also have neural correlates. Allen (2007) scanned patients with auditory hallucinations, compared to a control. Lower activation levels were found in superior temporal gyrus and anterior cingulate gyrus of hallucination group. Reduced activity in these parts of the brain is a neural correlate for auditory hallucinations.
• • genetic influence data is reliable
  • genetic susceptibility evidence such as the Gottesman study (1991). (Tenari 2004) adoption studies - children who have biological parents with SZ have a heightened risk of SZ and can still get when adopted into parents with no history.
  • studies - influence of genetics in the development of SZ - Gottesman studies shows concordance rates 48% for MZ twins - influence of nurture and environment in thewe predispositions such as family dysfunction.
  • the evidence is reliable, doesn’t mean that SZ is caused by entirely genetic factors, just increase the risk.
• • the role of environment is unclear
  • evidence supporting the role of biological factors in SZ is overwhelming. However there is evidence to show environmental factors including family functioning during childhood.
  • Evidence has been found in the concordance rate of MZ and DZ twins not being higher than 48%.
  • further genetic influence can be found between paternal age and risk of SZ. Increases from 0.7% with dad <25 to 2% for dad 50—Therefore environmental factors must also be equally researched to both prevent and reduce the impact of SZ in the population.
• dopamine explanation is reductionist.

  • evidence - dopamine agonists have shown to make the symptoms of SZ worse (Curran 2004).studies show how antipsychotic drugs which reduce activity of dopamine ease symptoms (Tauscher 2014)
  • evidence show =not full pictures as genes found in Ripke study produce other neurotransmitters such as Glutamate. glutamate system regulates the amount of dopamine released, shown this controls the amount of GABA released, so how much dopamine is released.
  • only dopamine doesn’t give the full picture of the role neurotransmitters in SZ (Moghadden and Jarvis 2012)
• neural correlates - problem with causation

  • lots of neural correlates with both negative and positive symptoms, but are they actually causing SZ?
  • e.g. correlation between levels of activity in the Venda striatum and negative symptoms of SZ. could be something wrong with this part of brain and less info is passing through = less activity. or it could be another factors causing negative symptoms and activity in the brain.
  • therefore, we can’t be sure that just because there is a correlation this means this is a cause of the symptoms. this is too simple meaning the real cause is not identified