Schizophrenia: Biological Explanation

Question 1

What is the genetic explanation for schizophrenia?

Answer 1

• Early research by Meehl proposed that a single gene (schizogene) was responsible for schizophrenia. Researchers now believe schizophrenia is polygenic, meaning many different candidate genes may be involved in the disorder. One of the candidate genes for schizophrenia that has received considerable attention by researchers is COMT gene.

Question 2

What is the dopamine hypothesis?

Answer 2

• The dopamine hypothesis explained that the positive symptoms of schizophrenia were due to hyperactivity of dopaminergic neurons in a part of the brain called the reward pathway. The excessive activity of these dopaminergic neurons is due both to higher levels of dopamine being released by Presynaptic neurons but also greater numbers of a type of dopamine receptor called D2 receptor. Researchers later added to the dopamine hypothesis. In this revised dopamine hypothesis, it was claimed that the negative symptoms of schizophrenia could be explained by hypo activity of dopaminergic neurons in a part of the brain responsible for decision making called the prefrontal cortex.

Question 3

Explain neural correlates as an explanation for schizophrenia.

Answer 3

• Researchers investigating the neural correlates of schizophrenia seek to identify abnormalities in the structure and function of regions of the brain that correlate with the positive and negative symptoms of schizophrenia.
• Eg. Patients with schizophrenia experiencing avolition have been found to exhibit reduced activation in the ventral striatum, a brain region involved in anticipating rewards. The reduced activation may explain their lack of motivation for goal-directed behaviour.

Question 4

What research support is there for the genetic basis for schizophrenia?

Answer 4

Joseph carried out a meta analysis of schizophrenia twin studies. The analysis revealed that the concordance rates for monozygotic twins was 40.4% and 7.4% for dizygotic twins. Since MZ twins share more genetic similarity than DZ twins, disorders with a genetic basis are
expected to be more common in MZ twins. Therefore, the study’s finding of higher concordance rates
for MZ twins compared to DZ twins suggests a genetic basis for schizophrenia. However, this finding
shows that genetics alone cannot explain schizophrenia, as concordance rates for genetically identical
MZ twins are not 100%. This suggests environmental factors also contribute, indicating the genetic
explanation is only part of the overall explanation for schizophrenia. This study’s support for the genetic
explanation is strong as it is based on a meta-analysis. Since this method combines data from multiple
studies, this study’s overall sample is more likely to be representative of people with schizophrenia. This
enhances the generalisability of this study’s conclusions about the (partial) genetic basis for
schizophrenia. However, this study’s support for the genetic basis of schizophrenia is limited by its
reliance on twin studies. Critics argue that due to their perceived similarity, identical twins may be
treated more similarly than non-identical twins. This makes it unclear whether higher concordance rates
in identical twins are due to genetics or the environment, undermining the study’s internal validity and
its support for genetics in schizophrenia.

Question 5

What evidence to support the dopamine hypothesis as an explanation for schizophrenia?

Answer 5

For example, antipsychotic medications which block the action of dopamine
(dopamine antagonists) have been used to effectively treat the positive symptoms of
schizophrenia. This effect of antipsychotics supports the dopamine hypothesis because it
demonstrates a link between dopamine hyperactivity and the positive symptoms of
schizophrenia. However , Noll (2009) has argued that since antipsychotics do not reduce
hallucinations and delusions in about one third of people with schizophrenia, then
dopamine alone cannot be the explanation for the positive symptoms of schizophrenia. This
suggests the dopamine hypothesis offers a partial explanation for schizophrenia. Moreover,
this finding only provides support for the dopamine hypothesis, and offers no support or
challenge to the revised dopamine hypothesis, which explains negative symptoms.

Question 6

How has research identified a neural correlation for the positive symptoms of schizophrenia?

Answer 6

Using fMRI, Allen (2007) found that compared to controls, schizophrenic patients
experiencing auditory hallucinations had abnormally low activity in the superior temporal
gyrus, a brain region associated with the identification of inner speech.
This study provides clear evidence that abnormalities in the superior temporal gyrus are
associated with the symptom of auditory hallucinations of schizophrenia, suggesting this
brain region is a neural correlate for this symptom. There is a supporting functional
explanation that corroborates this study’s identification of the superior temporal gyrus as a
neural correlate: since the superior temporal gyrus is responsible for the identification of
inner speech, abnormalities within this brain region could lead a person to misattribute
their inner speech to an external source, resulting in the experience of an auditory
hallucination. However, this research only provides evidence of a correlation between
hallucinations and the superior temporal gyrus. We cannot necessarily assume the
abnormal functioning of this part of the brain causes hallucinations, as the direction of
causation could run the other way (perhaps experiencing hallucinations causes this part of
the brain to function abnormally).

Question 7

What is a problem with the biological explanation?

Answer 7

Biological explanations for schizophrenia are biologically reductionist as they seek to
explain complex phenomena (i.e., the symptoms of schizophrenia) purely in terms of the
contribution of features of our biology, such as our genes, dopamine levels and abnormal
functioning of parts of the brain.
This reductionist approach inevitably simplifies and, in doing so, it ignores the
interaction with other relevant levels of explanation, such as the role of stressor in our
environment. Moreover, this reductionist approach is at odds with holistic explanations,
which consider the role of all relevant factors. Given the complexity of schizophrenia,
perhaps this approach, which avoids the oversimplification resulting from reductionist
explanations, would be better.