6.2: Biological explanations for schizophrenia

Question 1

Describe and evaluate biological explanations for schizophrenia (16 marks)

Answer 1

Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia

Question 2

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.

Answer 2

It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia

Question 3

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.

Answer 3

It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition

Question 4

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact,

Answer 4

In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.)

Question 5

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia

Answer 5

Another biological explanation for schizophrenia is the dopamine hypothesis

Question 6

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version

Answer 6

The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex

Question 7

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
Example

Answer 7

For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia

Question 8

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

First AO3 PEEL paragraph

Answer 8

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis

Question 9

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
Example

Answer 9

For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity

Question 10

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
What does this suggest?

Answer 10

This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia

Question 11

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However,

Answer 11

However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia

Question 12

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
Why is this?

Answer 12

This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters

Question 13

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.

Answer 13

Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012)

Question 14

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
What does this show?

Answer 14

This shows that the dopamine hypothesis is not valid and so other biological explanations are better

Question 15

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia

Answer 15

Another biological explanation for schizophrenia is neural correlates

Question 16

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.

Answer 16

One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved

Question 17

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
Why is this?

Answer 17

This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms

Question 18

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore,

Answer 18

Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007)

Question 19

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al.

Answer 19

Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group

Question 20

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus,

Answer 20

Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations

Question 21

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

Second AO3 PEEL paragraph

Answer 21

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia

Question 22

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
Why is this?

Answer 22

This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms

Question 23

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
Example

Answer 23

For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area

Question 24

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.

Answer 24

It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia

Question 25

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is

Answer 25

We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly

Question 26

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly.

Third AO3 PEEL paragraph

Answer 26

The third AO3 PEEL paragraph is that Regardless, there does seem to be a unifying underlying cause of this illness/group of illnesses

Question 27

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly.

The third AO3 PEEL paragraph is that Regardless, there does seem to be a unifying underlying cause of this illness/group of illnesses.

Answer 27

Imbalances of neurotransmitters affect activation of areas of the brain.
This is the proximate cause

Question 28

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly.

The third AO3 PEEL paragraph is that Regardless, there does seem to be a unifying underlying cause of this illness/group of illnesses.
Imbalances of neurotransmitters affect activation of areas of the brain.
This is the proximate cause.
Ultimately,

Answer 28

Ultimately, behind this is a genetic vulnerability, which may be triggered by environmental stressors, as looked at by the diathesis-stress model

Question 29

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly.

The third AO3 PEEL paragraph is that Regardless, there does seem to be a unifying underlying cause of this illness/group of illnesses.
Imbalances of neurotransmitters affect activation of areas of the brain.
This is the proximate cause.
Ultimately, behind this is a genetic vulnerability, which may be triggered by environmental stressors, as looked at by the diathesis-stress model.
Who is this supported by?

Answer 29

This is supported by Tienari et al. (2004), who found that a child-rearing style characterised by high levels of criticism and conflict and low levels of empathy was implicated in the development of schizophrenia, but for the children with a high genetic risk only

Question 30

Describe and evaluate biological explanations for schizophrenia (16 marks).
Candidate genes are individual genes believed to be associated with the risk of inheritance of schizophrenia.
It appears that schizophrenia is polygenetic, meaning that a number of different genes may all work in combination to produce schizophrenia.
It also appears that schizophrenia is aetiologically heterogeneous, meaning that different combinations of candidate genes can lead to an individual developing the condition.
In fact, 108 separate genetic variations are associated with an increased risk of schizophrenia (Ripke et al.).

Another biological explanation for schizophrenia is the dopamine hypothesis.
The original version focused on the role of high levels or activity of dopamine (hyperdopaminergia) in the subcortex, but more recent versions of the dopamine hypothesis have instead focused on abnormal dopamine systems in the brain’s cortex.
For example, Goldman-Rakic et al. (2004) identified a role for low levels of dopamine (hypodopaminergia) in the prefrontal cortex in the negative symptoms of schizophrenia.

The first AO3 PEEL paragraph is that there is research support for the dopamine hypothesis.
For example, Curran et al. (2004) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers and Tauscher et al. (2014) found that antipsychotic drugs, on the other hand, work by reducing dopamine activity.
This suggests that dopamine plays an important role in schizophrenia and so is a valid explanation of schizophrenia.
However, there is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.
This is because although dopamine is likely to be one important factor in schizophrenia, so are other neurotransmitters.
Much current recent in psychology has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt, 2012).
This shows that the dopamine hypothesis is not valid and so other biological explanations are better.

Another biological explanation for schizophrenia is neural correlates.
One negative symptom is avolition, which involves the loss of motivation, and certain regions of the brain, for example the ventral striatum, are believed to be particularly involved.
This is because Juckel et al. (2006) measured activity levels in the ventral striatum in schizophrenia sufferers and found lower levels of activity than those observed in a control group.
They found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia, but positive symptoms also have neural correlates, as shown by Allen et al. (2007).
Allen et al. scanned the brains of patients experiencing auditory hallucinations and compared them to a control group as they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group.
Thus, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

The second AO3 PEEL paragraph is that the varied causal biological explanations for schizophrenia invalidate the classification and diagnosis of schizophrenia.
This is because it is possible for two people to be diagnosed with schizophrenia without sharing any symptoms.
For example, avolition is correlated with lower activation of the ventral striatum (Juckel) and is a negative symptom of schizophrenia.
However, auditory hallucinations have been found to be associated with hyperdopaminergia in Broca’s area.
It is possible that the underlying causes are so varied, because we are in fact looking at the symptoms of illnesses other than schizophrenia.
We know that there is high co-morbidity and perhaps this illustrates we are actually looking at underlying causes of bipolar disorder or other illnesses and simply diagnosing incorrectly.

The third AO3 PEEL paragraph is that Regardless, there does seem to be a unifying underlying cause of this illness/group of illnesses.
Imbalances of neurotransmitters affect activation of areas of the brain.
This is the proximate cause.
Ultimately, behind this is a genetic vulnerability, which may be triggered by environmental stressors, as looked at by the diathesis-stress model.
This is supported by Tienari et al. (2004), who found that a child-rearing style characterised by high levels of criticism and conflict and low levels of empathy was implicated in the development of schizophrenia, but for the children with a high genetic risk only.
What does this show?

Answer 30

This shows that an interactionist approach should be adopted, since it is a more complete explanation of schizophrenia