Biological explanations Flashcards
What are the 3 biological explanations for schizophrenia?
- Genetic explanations (inheritance and specific genes)
- Dopamine hypothesis
- Neural correlates
Explain inheritance as a biological explanation for schizophrenia and the evidence that supports it
Inheritance suggests that schizophrenia runs in the family and is genetic. Family studies indicate that the closer the genetic relationship with someone with schizophrenia, the more likely you are to develop the disorder.
Evidence:
- Gottesman found that the chances of first degree relatives developing schizophrenia is 12%. If both parents have schizophrenia then there is a 40% chance that their child will develop schizophrenia.
- Cardno et al found a 40% concordance rate in MZ twins compared to 5.3% in DZ twins which shows that individuals with identical genetic make-up (MZ twins) have an increased risk of developing schizophrenia than DZ twins who only share half of their genes.
What is a problem with using twin studies/comparing concordance rates between people in the same family?
The problem is that they share the same environment. Instead we can isolate the environmental and genetic effects by using adoption studies and comparing them with biological and adoptive parents.
Explain the evidence of adoption studies.
Heston - Compared 47 children of schizophrenic mothers who had been fostered or adopted in the first month of their life with a control group of 50 children who had been raised in the same homes as these children.
Findings - None of the children from the control group developed schizophrenia but 17% of the children with schizophrenic biological mothers developed schizophrenia. Shows that having the same genetic material as a schizophrenic can increase your chances of gaining schizophrenia.
Explain specific genes as a biological explanation for schizophrenia and the evidence that supports it
Schizophrenia is polygenic meaning multiple genes are involved in schizophrenia and is also aetiologically heterogenous meaning that schizophrenia is caused by different candidate genes.
Evidence:
- Miyakawa et al studied the DNA from families affected by schizophrenia and found that those with the disease were more likely to have a defected version of a gene called PPP3CC which is associated with the production of calcineurin which regulates the immune system.
- Sherrington et al found a gene located on chromosome 5 which has been linked to schizophrenia in a small number of extended families who had the disorder.
Evaluate the genetic explanation
- The concordance rate for MZ twins who are genetically identical is not 100% which implies that genetics play a factor in developing schizophrenia but they are not the only factor influencing schizophrenia. By focusing on only one factor being genes, the explanation develops a biological reductionist approach since other factors are not considered e.g. family dynamics. The very narrow approach cannot explain why if one MZ twin has schizophrenia why the other twin only has a 40-60% risk of developing it too.
- It is difficult to separate the impact of nature and nurture. Both family and twin studies investigate individuals who have grown up in the same environment which could be the factor that increases concordance rates. The higher concordance rates of MZ twins could be because they are treated more similarly than DZ twins and not due to their genetics. This makes it harder to differentiate between genetic and environmental influences.
What is dopamine?
Chemical neurotransmitter in the brain which causes neurons to fire and transmits signals between the neurons in the brain
State the original and new dopamine hypothesis
Original - Schizophrenia is caused by excess activity of dopamine which causes neurons that respond to dopamine to fire too often leading to a message over load that can cause symptoms of schizophrenia.
New - Schizophrenia is caused by a high density of dopamine receptors and a high level of sensitivity of dopamine receptors which causes neurons to fire too often. Too much dopamine released into the synapse causes onset of schizophrenia.
Explain the difference between the original and the new dopamine hypothesis including brain structures.
Original
- hyperdopaminergia in subcortex
- focuses on high levels of dopamine in the subcortex (central areas of the brain) E.g. Broca’s area is responsible for speech production so a high level of dopamine in this area could result in speech poverty.
New
- hypodopaminergia in cortex
- focuses on abnormal dopamine systems in the brains cortex specifically the pre-frontal cortex which is responsible for thinking and decision making which could explain negative symptoms
Who updated the dopamine hypothesis and why?
Davis et al updated the hypothesis because high levels of dopamine are not found in all schizophrenics. Also, the drug clozapine used to treat schizophrenia has little doapmine-blocking activity and still works efficiently against treating the illness.
According to the new model how are positive and negative symptoms caused?
Positive - overactivity of the mesolimbic pathway
Negative - dysfunction of mesocortical pathway
Evaluate the dopamine hypothesis
- One strength is that it has practical applications because it has led to the development of effective treatments such as the drug clozapine.
- One weakness is that dopamine abnormalities is not present in all schizophrenics, especially those with negative symptoms. Problems with dopamine seem to be associated with positive symptoms which means that it only explains certain aspects of the illness.
What is the neural correlates explanation for schizophrenia?
Schizophrenia is caused by enlarged ventricles which are fluid-filled gaps between brain areas that are associated with damage to central brain areas and the prefrontal cortex.
How does neural correlates explain negative symptoms?
The ventral striatum is involved with reward anticipation. Schizophrenics have been found to have less activity in this region which causes negative symptoms such as avolition.
Research into neural correlates
Juckel measured activity in the ventral stratium in schizophrenics and found a negative correlation between activity levels and the severity of negative symptoms which means activity in the ventral stratium is neural correlate of the negative symptoms of schizophrenia.
