1. Biological explanations
Schizophrenia
Biological explanations

2. Homework Revise for paper 1 mock (19th Nov) If you failed paper 1 mock
(19th Nov 9am-11pm room 219)
All groups: finish peer review/features of science if not completed on Friday

3. Starter: ABC

4. Objectives To be able to…
Describe the following biological explanations:
General Genetic Link
Neural Correlates
Dopamine hypothesis
Evaluate each explanation with research
Challenge:
Apply knowledge of the biological explanations to exam questions.

5. What does this tell us about the causes of schizophrenia?
Starter
More than 100 genetic regions have been found to be involved in schizophrenia, many of which were not previously linked to the condition.
Researchers say the finding uncovers the biological mechanisms causing the severe psychiatric disorder, and could lead to new treatments
One hundred and eight locations (loci) in the human genome were linked to schizophrenia, 83 of which were previously unknown. The study, published in Nature, noted that many of the genes were expressed in the brain, thus 'providing biological plausibility for the findings'. Three-quarters of the loci coded for proteins, including the dopamine receptor (which most current schizophrenia medications target), as well other genes involved in brain signalling.
What does this tell us about the causes of schizophrenia?

6. Question: Who do we study to find out a genetic link and why?
General Genetic link
Question: Who do we study to find out a genetic link and why?

7. Biological: Always start with ‘Twin Studies’
Why start with Twin studies?….. explain
Twin studies have identified strong concordance rates:
MZ = 0.40
DZ = 0.07
General Population = 0.01 (1% risk)
Point of interest: If your partner has schizophrenia your risk is twice that of the general population (2%: can you suggest why?)

8. Biological explanations (A01)
Read the content on page and answer the following exam questions:
According to the general genetic hypothesis what increases your chance of developing the disorder?
What is the likelihood of developing the disorder in the general population?
According to Gottesman (1991), what is the percentage concordance rate of developing the disorder if one parent has the disorder?
What methods are used to determine the genetic influence on schizophrenia?
What does concordance rate mean?
What were the findings of Gottesman’s study of MZ and DZ twins (1966)? What does this suggest about a genetic link in schizophrenia?
What were the results of Kety’s adoption study?
Why does it help our understanding of genetics to look at children brought up away from their biological parents?
Name the specific gene(The Genome project) identified that causes schizophrenia.?
There is strong evidence that shows schizophrenia is the result of multiple factors (genes + environment). This is also known as the diathesis stress model. How does the diathesis stress model explain schizophrenia?

9. Explanation 1: Genetics
What does the bar graph to the left show about the relationship between genetics and schizophrenia?
How can we evaluate the use of twin studies to look at the genetic basis of schizophrenia?
Challenge: How far do you think this data is valid?
Gottesman (1991)

10. There is overwhelming evidence for the idea that genetic factors make some people more vulnerable to developing schizophrenia than others.
However, this does not mean that schizophrenia is entirely genetic. The diathesis-stress model may be a better way to explain the development of schizophrenia, where individuals inherit different levels of genetic predisposition, but ultimately it is environmental triggers that determine whether individuals go on to develop schizophrenia.
Twin and family studies fail to consider the contribution of shared environmental influences on development of the disorder.
If genes caused schizophrenia on their own, concordance rates between MZ twins would be 100%, which they are not. Twin studies also produce confusing evidence, with concordance rates for MZ twins ranging from 58% down to a slow as 11%.

11. Evaluation: twin studies (A03)
Finish off the sentences evaluating the genetic explanation of schizophrenia on page 25 Extension (A/A*): research the C4 gene that has been found this year to increase the risk of schizophrenia
Nature vs. Nurture
Determinism
Methodological Flaws
Are MZ twins treated more similarly

12. Neural Correlates

13. Brain Areas
If there is a genetic link how does this lead to the symptoms?
It is likely that the genes are expressed in the brain.
Task: Watch the video and make notes on the neural explanation and dopamine hypothesis
Extension: what points can you use to evaluate the biological explanation?

14. Neural Correlates
Neural correlates are measurements of the structure or function of the brain that correlate with an experience, in this case schizophrenia.
Both positive and negative symptoms have neural correlates.
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 schizophrenia.

15. Enlarged Ventricles: negative symptoms
Read bottom of page 27
Johnstone et al (1976) first studied this using CT scans. They found significant ventricular enlargement in a group of chronic schizophrenia sufferers. This research has since been replicated.
Then answer the following questions.
1. What is a ventricle?
2. What are they filled with?
3. If the ventricles are larger what does this mean for brain tissue?
Synoptic – the brains of children suffering neglect and abuse often show reduced brain tissue and increased ventricles

16. Neural Correlates: Ventricles
People with schizophrenia have abnormally large ventricles in the brain.
Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste.
This means that the brains of schizophrenics are lighter than normal.
The ventricles of a person with schizophrenia are on average about 15% bigger than normal (Torrey, 2002).

17. Suddath et al. (1990).
Supporting evidence for the brain structure explanation comes from further empirical support from
He used MRI (magnetic resonance imaging) to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic.
The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs.
This suggests that there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.

18. Extension (A/A*) Neural Correlates: ventral striatum
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 et al (2006) measured activity levels here and found lower levels of activity in schizophrenics compared to controls.

20. Extension handout: linking Broca and Wernicke area to hallucinations
Positive symptoms
Allen et al. (2007) found that positive symptoms also have neural correlates.
They scanned the brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
We can thus say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.
Extension handout: linking Broca and Wernicke area to hallucinations

21. Damage to the Cerebral Cortex.
The dorsolateral prefrontal cortex.
Supporting cells (glial) in this area may be affected in schizophrenia. Thin impairs problem solving and interpretation of deception.

22.
Problems completing this task can be caused by underactivity in the frontal lobe. Patients with schizophrenia may find this task difficult

23. Evaluation of Brain Areas (A03)
Improved technology allows us to study the brain.
Is it a cause or an effect?
Extension: finish off the evaluation point
A weakness of the neuroanatomical explanations is that it is biologically deterministic…
Write up these points as evaluation of brain areas associated with schizophrenia. (page 30)

24. A strength of the research into enlarged ventricles has high reliability. The reason for this is because the research is carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the limbic system and the temporal lobe. This suggests that if this research was tested and re-tested the same results would be achieved adding credibility to a biological basis of SZ.

25. However, the neuroanatomical explanation does not answer the question of causation- does the unusual activity in that region cause the symptoms or does the disorder itself cause these brain differences. For example, it appears to be schizophrenics who do not respond to medication who mainly exhibit enlarged ventricles. This could mean that it is an effect of suffering from schizophrenia over a long period that leads to the physical brain damage rather than brain damage leading to schizophrenia. Ho et al. (2003) performed MRI scans on recent-onset schizophrenics and re-scanned them 3 years later. They found evidence of brain damage in the recent- onset patients, which worsened over time, especially in the frontal lobes, which correlated with an increase in the severity of their symptoms. This suggests brain damage does increase in schizophrenics over time.

26. A weakness of the neuroanatomical explanations is that it is biologically deterministic…

28. Outline two biological explanations of schizophrenia (8 marks)
Exam focus
Outline two biological explanations of schizophrenia (8 marks)
Switch with your partner. In a different colour, can you improve on the answer?

29. Exam focus
Louise comes from a family with a history of schizophrenia, as both her grandfather and an aunt have been diagnosed with the disorder. Louise's father has recently died from cancer and she has moved out of her family home to start university. Although she has always been healthy in the past, she has begun to experience symptoms of schizophrenia, such as delusions and hallucinations.
Using your knowledge of schizophrenia, explain why Louise is now showing symptoms of schizophrenia (4)

30. Model answer
There is a history of schizophrenia in Louise's family so Louise could have inherited a genetic vulnerability to developing the disorder. This may have been triggered by the stressful life events she is experiencing. She has recently lost her father and she has left home to start university. These are both significant life events that could trigger a genetic predisposition to schizophrenia. This is an interactionist explanation for the development of schizophrenia and is known as the diathesis-stress model of mental illness.

31. Dopamine Hypothesis

32. Objectives To be able to…
Describe the dopamine hypothesis as an explanation of schizophrenia
Compare how the revised dopamine hypothesis differs from the original hypothesis
Evaluate using PEEL paragraphs the DH
Challenge
To be able to evaluate the biological explanations as a whole and answer a 16 mark exam question

33. Can you label the different parts.
Starter
What is this?
Can you label the different parts.

34. The Dopamine Hypothesis
How can high levels of dopamine influence behaviour?
The three neurotransmitters involved in schizophrenia are dopamine, glutamate and serotonin.
Find out the role of each neurotransmitter

35. The 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 schizophrenia.
Dopamine is particularly important in the functioning of several brain systems that may cause symptoms of schizophrenia – in particular the cortex and subcortex.

36. The Dopamine Hypothesis
Dopamine is a neurotransmitter involved in initiating movement and has a major role in reward motivated behaviour. The dopamine hypothesis states that schizophrenia is caused by an excess of the neurotransmitter dopamine in certain areas of the brain. Messages in the brain that transmit dopamine either fire to easily or too often. This leads to the characteristic positive symptoms of schizophrenia. This could be because a person has an increased number of D2 receptors in the brain, especially in subcortical areas such as the limbic system.

37. Dopamine, Dopamine, Dopamine…
Hyperdopaminergia = Excessive levels of dopamine in the Subcortex & Broca’s Area
(high level of sensitivity to dopamine receptors: neurons that respond to dopamine fire too often and transmit too many messages)
Hypodopaminergia = Low levels of dopamine in the prefrontal cortex.

38. The Dopamine Hypothesis
The initial dopamine hypothesis was identified with the development and use of antipsychotics.
These drugs reduced the symptoms of schizophrenia (positive symptoms) but how did they work?
Our knowledge of the effects of these drugs and of recreational drugs led to the first Dopamine hypothesis

39. This is a simplistic view and the dopamine hypothesis was revised.
So the dopamine hypothesis states that it is an excess of dopamine in certain regions of the brain such as the limbic system, that causes the symptoms. Messages in the brain that transmit dopamine either fire to easily or too often. This leads to the characteristic positive symptoms of schizophrenia.
This is a simplistic view and the dopamine hypothesis was revised.

40. Revised Dopamine Hypothesis
Davis et al (1991) stated that in schizophrenia, positive symptoms were caused by increased dopamine activity in subcortical areas such as the mesolimbic system.
Negative symptoms are caused by a deficit of dopamine activity in the prefrontal cortex (mesocortical pathway).

43. Create an acronym to help you remember the DH
Acronym creation
Create an acronym to help you remember the DH

44. Extension Are there other Neurotransmitters Involved?
Glutamate
The receptor for glutamate is NMDA and is present in areas of the brain involved in learning and memory.
If glutamate levels are low it can cause an increase in dopamine.
Although reduced NMDA functioning is present at birth. It becomes most problematic around puberty. This fits in with the timing of schizophrenic symptoms.

45. Extension: Serotonin Remember the basal ganglia?
In post mortem studies of people with schizophrenia – this area has been shown to have higher levels of serotonin.
High levels of serotonin cause a reduction in dopamine and so could lead to negative symptoms.

46. Question
Outline the dopamine hypothesis as a biological cause of schizophrenia (6)

47. Dopamine is a neurotransmitter involved in initiating movement and has a major role in reward motivated behaviour. The dopamine hypothesis states that schizophrenia is caused by an excess of the neurotransmitter dopamine in certain areas of the brain. This could be because a person has an increased number of D2 receptors in the brain, especially in subcortical areas such as the limbic system. It is thought that messages from neurons that transmit dopamine either fire to readily or too often leading to the characteristic symptoms of schizophrenia such as hallucinations or delusions. However, the revised dopamine hypothesis could better explain the presence of negative symptoms. It states that the positive symptoms of schizophrenia are caused by over activity of the dopamine system in subcortical areas of the brain such as the mesolimbic pathway. Whereas the negative symptoms could be caused by a deficit of dopamine activity in the mesocortical pathway. The revised dopamine hypothesis can explain why some patients do not respond to traditional antipsychotic drugs which simply block the dopamine receptors.

48. Discuss biological explanations for schizophrenia. (Total 16 marks)
Essay
Discuss biological explanations for schizophrenia. (Total 16 marks)
Identify the A01/A02
Using the essay create a plan for the title (deconstruct the essay to its main points
Outline strengths and weaknesses of the essay.

49. ABC A holds the key terms.
B talks for one minute about what we have learnt.
C talks further for one minute trying to fill in the gaps.
A ticks off any key terms used in context.
Then A reads off the rest of the key terms and you contextualise them as a group.