Biological Explanations of Schizophrenia

  • Created by: nwheway
  • Created on: 06-03-19 14:16
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  • Biological Explanations of Schizophrenia
    • Generic Basis of Schizophrenia
      • Schizophrenia Runs in Families
        • This is a weak link as families share aspects of their environment as well as some of their genes.
        • Gottesman (1991) found that identical twins had a 48% chance of developing Sz, whereas non-identical twins had a 17% chance
      • Candidate Genes
        • Individual jeans that are associated with the risk of inheritance.
        • Polygenic - There are a number of genes that are linked to the increase risk of Sz.
        • Ripke et al (2014) found that there were 108 separate genetic variations associated with the increased risk of Sz.
          • Genes found to be associated included those coding for the functioning of a number of neurotransmitters including dopamine.
    • The Dopamine Hypothesis
      • Neurotransmitters
        • The brains chemical messengers appear to work differently in the brain of a patient with Sz.
      • Hyperdopaminergia in the subcortex
        • High levels of dopamine in the subcortex
        • Excess of dopamine in Broca's area may be associated with speech poverty.
      • Hypodopaminergia in the cortex
        • Low levels of dopamine in the cortex
        • Low levels of dopamine in the prefrontal cortex may be associated with negative symptoms of Sz.
    • Neural Correlates
      • Measurements of the structure or function of the brain that correlate with an experience.
      • Neural Correlates of Negative Symptoms
        • Avolition involves the less of motivation. The ventral striatum is particularly involved in this. Juckle er al (2006) found that lower levels of activity were found in Sz patients.
          • This means that there is a negative correlation between the ventral striatum and the severity of overall negative symptoms
      • Neural Correlates of Positive Symptoms
        • Allen et al (2007) found that in patients with auditory hallucinations, there was lower activity levels in the superior temporal gyrus and anterior cingluate gyrus
    • AO3
      • Multiple Sources of Evidence for Genetic Susceptibility
        • Gottesmans study clearly shows how the genetic similarity and shared risk of Sz are closely related. Adoption studies such as that by Tienari show that children of Sz sufferers are still at heightened risk of Sz if adopted into families with no history of Sz. Thus, there is overwhelming evidence for the idea that genetic factors make some people more vulnerable to developing Sz than others.
          • This does not mean that Sz is entirely genetic. There are a number of risk factors in the environment associated with Sz.
      • Mixed Evidence for the Dopamine Hypothesis
        • Dopamine agonists like amphetamines that increase the levels of dopamine make Sz worse and can produce Sz-like symptoms in non-sufferers. Antipsychotic drugs work by reducing dopamine in Sz. Both kinds of drug studies suggest an important role for dopamine in Sz. There is also evidence that suggests that dopamine does not provide a complete explanation for Sz. Some of the genes identified by Ripke code for the production of other neurotransmitters.
          • So it appears that although dopamine is likely to be one important factor, so are other neurotransmitters.
      • The Causation - Correlation Problem
        • Neural correlate studies are useful in falgging up particular brain systems that may not be working normally, this kind of evidence leaves some important questions unanswered. most importantly, whether the unusual activity causes the symptom. for example, it is possible that the negative symptom is caused by the unusual activity in the ventral striatum but it is also possible that unusual activity in the ventral striatum is caused by the negative symptom.
      • The Role of Mutation
        • Sz can take place in the absence of a family history of the disroder. one explanation for thiis is mutation in parental DNA, for example in paternal sperm. this can be caused by radiation, poison or viral infection. evidence for the role of mutation comes from a study showing a positive correlation between paternal age and risk of Sz. increasing from around 0.7% in father under 25 to over 2% in fathers over 50.
      • The Role of the Psychological Environment is Important but Unclear.
        • The evidence supporting the role of biological factors in Sz is overwhelming. However there is also evidence to suggest an important tole for environmental factors, including psychological ones such as family functioning during childhood. after all, the probability of developing Sz even if your identical twin has it is less than 50%.

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