Biological Explanations Flashcards
What evidence suggests that schizophrenia runs in families?
There is a strong relationship between genetic similarity of family members and likelihood of both developing schizophrenia. Gottesman’s family study found MZ twins have 48% shared risk of schizophrenia. DZ twins have a 17% shared risk and siblings have a 9% shared risk.
What evidence shows that schizophrenia is polygenetic and aetiologically heterogeneous.
- Different individual gene confers a small increased risk of schizophrenia (i.e. It is polygenetic)
- Different combinations can lead to schizophrenia (i.e. It is aetiologically heterogeneous).
Ripke et al studied 37,000 patients and found 108 separate genetic variations associated with the increased risk; many coded for the dopamine neurotransmitter.
How is high dopamine activity linked to the subcortex?
Hyperdopaminergia is high levels of dopamine activity in the subcortex (central areas of the brain) which is associated with hallucinations and poverty of speech (e.g. Excess of dopamine receptors in Broca’s area).
What is the key role played by dopamine?
Dopamine is widely believed to be involved in schizophrenia because it is featured in the functioning of brain systems related to the symptoms of schizophrenia.
Where is there to little dopamine?
Hypodopaminergia: low levels of dopamine in the prefrontal cortex which is responsible for thinking and decision making.
How is brain activity linked with symptoms?
Neural correlates are measurements of the structure or function of the brain that correlate with the positive or negative symptoms of schizophrenia.
What can hallucinations be explained by in terms of neural correlates?
Allen et al found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus.
What can avolition be explained by in terms of neural correlates?
Ventral striatum is involved in anticipation of reward (related to motivation). Loss of motivation (avolition) in schizophrenia may be explained by low activity levels here. Juckel et al found a negative correlation between ventral striatum activity and overall negative symptoms.
Strength: strong evidence for genetic vulnerability to schizophrenia.
The Gottesman family study clearly shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies (Tienari et al) show children of people with schizophrenia are still at heightened risk of schizophrenia if adopted into families without a history of schizophrenia. So schizophrenia may not be entirely genetic, but there is overwhelming evidence that genetic factors make some people more vulnerable.
Limitation: mixed support for the dopamine hypothesis.
Dopamine agonists (eg amphetamines) that increase dopamine activity can induce schizophrenia-like symptoms on people without schizophrenia. Antipsychotic drugs that lower dopamine can be effective in reducing symptoms. However, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate. This suggests that dopamine cannot provide a complete explanation for schizophrenia and that it is just one important factor.
Limitation: correlation-causation problem.
The question that remains is whether unusual activity in the brain causes the symptoms or whether there are other possible explanations for the correlation. A negative correlation may suggest that low activity in the ventral striatum causes avolition. But it could be that avolition means that less information passes through the striatum resulting in the low activity. Therefore, although neural correlates exist, they tell us relatively little about the causes of schizophrenia.
Strength: the role of mutation supports the genetic explanation.
Schizophrenia can take place in the absence of family history of the disorder (e.g. Through mutation of paternal DNA in sperm cells caused by radiation, poison or viral infection). Brown et al found a link between paternal age (associated with risks of mutation) and risks of schizophrenia, increasing from 0.7% in fathers under 25 to 2% in fathers over 50. This evidence supports the importance of genetic factors in the development of schizophrenia.
Limitation: it is clear that the environment is also involved.
After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%. There is evidence that environmental factors (e.g. Family functioning in your childhood) can also play a role in the development of schizophrenia. This suggests that schizophrenia may be the result of a combination of biological and psychological approaches (as acknowledged by the interactionist approach).
