Biological Explanations for Schizophrenia

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1. What are the three main biological explanations for schizophrenia?
Genetic factors, the Dopamine hypothesis and Neural correlates
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2. How does the genetic explanation see schizophrenia as transmitted?
through hereditary means i.e. from genes passed on from family
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3. What is there believed not to be?
A single 'schizophrenia gene' - several genes involved which increase vulnerability
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4. How is the genetic explanation typically researched?
twin, family and adoption studies to assess concordance rates of developing schizophrenia. More recently Gene mapping
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5. Gottesman and Shields (1976)
Reviewed five twin studies = concordance rate of between 75 per cent and 91 per cent for MZ twins with severe schizophrenia suggesting genes play larger role in chronic forms of the disorder
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6. Torrey et al (1994)
Reviewing evidence from twin studies, found that if one MZ twin develops schizophrenia, 28 per cent chance that the other will too, supporting the idea that schizophrenia is inherited
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7. Gurling et al (2006)
Used evidence from family studies indicating that schizophrenia was associated with chromosome 8p21-22. Using gene mapping, the PCMI gene was implicated in susceptibility to schizophrenia, providing more evidence for genetics
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8. Benzel et al (2007)
Used gene mapping to find evidence suggesting NRG3 gene variants interact with both NRGI and ERBB4 gene variants to create a susceptibility to developing schizophrenia, suggesting genetic interaction.
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9. What are the strengths of the genetic explanation?
Findings from genetic studies provide evidence for the diathesis-stress model, where individuals inherit different levels of genetic predisposition to developing schizophrenia, gene mapping can identify high risk individuals
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10. What are the weakness of the genetic explanation?
Twin and family studies fail to consider environmental influences, if genes causes schizophrenia on their own CR would be 100 per cent, which it isn't, gene mapping can bring about socially sensitive and ethical concerns
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11. What is the Dopamine Hypothesis centred on?
The idea that the neurotransmitter dopamine is linked to the onset of schizophrenia
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12. What does dopamine do?
Increase the rate of firing of neurons during synapse, which enhances communication between neurons
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13. What did Snyder (1976) argue?
Argued that if too much dopamine is released during synapse it can lead to the onset of schizophrenia
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14. When did Snyder's theory develop?
The theory developed after it was discovered that phenothiazines, antipsychotic drugs that lessens symptoms of schizophrenia, seem to work by decreasing dopamine activity
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15. Why did Davis et al (1991) update the Dopamine Hypothesis?
High levels of dopamine are not found in all schizophrenics, and anti-schizophrenic drugs with little dopamine-blocking activity still work effectively against the disorder
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16. What did Davis et al suggest?
High levels of dopamine in the mesolimbic dopamine system are associated with positive symptoms, while high levels in the mesocortical dopamine system are associated with negative symptoms
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17. Why may the neurotransmitter glutamate be involved in schizophrenia?
dopamine receptors restrict the release of glutamate and there is reduced function of the NMDA glutamate receptor in people with schizophrenia
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18. How is the dopamine hypothesis studied?
Through post-mortems, brain scans, drug trails and animal studies
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19. Kessler et al (2003)
Used PET and MRI scans to compare people with schizophrenia with non-sufferers, finding that schizophrenics had elevated dopamine receptor levels specific brain areas.
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20. Iverson (1979)
Reported that post-mortems on people who had had schizophrenia found excess dopamine in the limbic system, suggesting that the neurotransmitter is involved in the disorder
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21. What are the weaknesses of the Dopamine Hypothesis?
Evidence is inconclusive as there is no consistent difference in dopamine levels between drug-free schizophrenics and non sufferers, several neurotransmitters might be involved in the development of schizophrenia, cannot explain length of recovery
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22. What did Healy (2000) believe about pharmaceutical companies?
They were keen to see the dopamine theory promoted, as they would make huge profits from manufacturing anti-schizophrenic drugs that inhibited dopamine production
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23. What is Dopamine more associated with?
Positive symptoms - so it may only contribute to certain aspects of the disorder. This could also suggest that there are several types of schizophrenia
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24. What can the Dopamine hypothesis be accused of being?
Oversimplistic
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25. What does the idea of neural correlates propose?
Abnormalities within specific brain areas may be associated with the development of schizophrenia
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26. How was evidence originally found for neural correlates?
post-mortems conducted upon brains of dead schizophrenics
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27. How is evidence found now?
Research now uses non-invasive scanning techniques, such as fMRIs, which give a picture of the brain in action through use of magnetic fields and radio waves
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28. What is this used to do?
compare to the brains of non-sufferers, to identify brain areas that may be linked to schizophrenia.
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29. How is comparison best achieved?
by giving tasks to participants associated with types of functioning know to be abnormal in schizophrenics, for example social cognition, thought processing and working memory tasks
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30. What is an important consideration about neural correlates?
whether brain abnormalities found in schizophrenics are caused by genetic factors or are a result of the disorder itself
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31. What can comparison of brains suggest?
a genetic link
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32. What was early research into neural correlates focused on?
schizophrenics having enlarged ventricles, these are especially associated with damage to central brain areas and this damage has been linked to negative symptoms.
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33. Johnstone et al (1976)
Found that schizophrenics had enlarged ventricles, while non sufferers did not which suggests schizophrenia is related to a loss of brain tissue.
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34. What did Weyandt (2006) report?
enlarged ventricles are associated with negative symptoms only, which implies enlarged ventricles cannot explain all symptoms and incidences of schizophrenia
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35. Boos et al (2012)
performed MRI scans on 155 schizophrenics, 186 of their non-schizophrenic siblings and 122 non-related schizophrenics, to find schizophrenic participants had less grey matter density and cortical thinning suggesting brain tissue has an effect.
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36. What is evidence against the effect of neural correlates?
Some non-schizophrenics have enlarged ventricles, while not all schizophrenics do, which goes against the idea of schizophrenia being linked to loss of brain tissue.
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37. What must be taken into consideration when assessing the role of brain abnormalities on schizophrenia?
environmental factors such as substance abuse and stress levels, which may also be having a damaging influence upon brain tissue.
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2. How does the genetic explanation see schizophrenia as transmitted?

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through hereditary means i.e. from genes passed on from family

Card 3

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3. What is there believed not to be?

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Card 4

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4. How is the genetic explanation typically researched?

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5. Gottesman and Shields (1976)

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