Biological explanations for SZ Flashcards
What are the two biological explanations for schizophrenia?
- Genetic basis of SZ
- neural correlates of SZ
What have family studies confirmed?
that the risk of SZ increases with genetic similarity to a relative with the disorder
What do Gottesman find in his large scale family study?
- found that SZ is more common in the biological relatives of someone with schizophrenia
e.g. someone with an aunt with SZ has a 2% chance of developing it, increasing to 9% if the individual is a sibling & 48% if they are an identical twin
What have genes have researchers identified associated with SZ?
- candidate genes > inherited genes that cause a disorder
- early research looked for one single genetic variation > but it appears that a number of different genes are involved > SZ is polygenic
- Ripke et al they discovered 108 separate genetic variations associated with slightly increased risk of SZ
- genes likely to be those coding for neurotransmitters like dopamine
What is concluded based on studies that identify different candidate genes involved in SZ?
- that SZ is aetiologically heterogenous > different combination of factors, including genetic variations can lead to SZ
How do psychologists explain those who have SZ without family history of the disorder?
- mutation in parental DNA which can be caused by radiation, poison or viral infection
- Brown et al > positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of SZ
What have researches identified since they don’t know what causes symptoms on a biological level and what is this?
- neural correlates > brain structure or activity that occurs in conjunction with an experience
What is the best know neural correlate for SZ?
- the neurotransmitter dopamine (DA) > has an excitatory effect
What is the original dopamine hypothesis based on?
- the discovery that antipsychotic drugs used to treat SZ caused symptoms similar to those with Parkinson’s disease > a condition associated with low dopamine levels (Seeman 1987)
What did psychologists conclude based on their discovery of AP drugs in the original DA hypothesis?
- that SZ might be the result of high levels of dopamine
- hyperdopaminergia in subcortical areas of the brain
- particularly in pathways from the subcortex to Broca’s area may explain symptoms like speech poverty and/or auditory hallucinations
What was proposed in the update dopamine hypothesis?
- Davis et al > proposed the addition of cortical hypodopaminergia > abnormally low dopamine in the brains cortex
- e.g. low dopamine in the prefrontal cortex (responsible for thinking) could explain cognitive problems (negative symptoms)
What has also been suggested in the updated dopamine hypothesis?
- that cortical hyperdopaminergia leads to subcortical hyperdopaminergia > both high & low levels of DA in different brain regions are part of the updated version
How does the current dopamine hypothesis explain the origins of abnormal dopamine function?
- Howes et al through both genetic variations & early experiences of stress make some people more sensitive to cortical hyperdopaminergia & hence subcortical hyperdopaminergia
What is a strength of the genetic explanation for SZ?
- real world application in genetic counselling
- If one or more potential parents have a relative with SZ, they risk having a child who would go on to develop the condition
- e.g. based on Gottesman’s study they will have a 2% probability if they have an uncle or aunt with schizophrenia, and a 6% probability if they have a half-sibling with it
- thus Genetic counselling involves informing potential parents of these probabilities so that they can make informed choices about whether to have children who risk having a poor quality of life if they develop schizophrenia
What is a limitation of the genetic explanation for SZ?
- clear evidence to show that environmental factors also increase the risk of developing schizophrenia
- these include both biological & psychological influences
- biological > birth complications and smoking THC-rich cannabis in teenage years
- psychological risk factors > childhood trauma e.g. Morkved et al found 67% of people with SZ & related psychotic disorder reported at least one childhood trauma
- genetic factors alone cannot provide a complete explanation for SZ
What is a strength of the role of neural correlates in SZ?
- support for the theory that dopamine is involved in SZ
- antipsychotic drugs e.g. chlorpromazine reduces dopamine activity & also reduce the intensity of symptoms
- and some candidate genes act on the production of dopamine or dopamine receptors
- real evidence that dopamine plays a role in the condition
> increases reliability of theory
What is a limitation of the dopamine hypothesis?
- is evidence for a central role of glutamate instead
- McCutcheon et al > Post-mortem & live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with SZ
- in addition, several candidate genes for SZ are believed to be involved in glutamate production & processing
- means that an equally strong case can be made for a role of other neurotransmitters
- decreases validity of theory > DA hypothesis ignores more influential neurotransmitter
