Schizophrenia - Biological explanations Flashcards
What are 3 AO1 points
Genetic explanations
Neural correlates
Dopamine hypothesis
Who looked at Genetic explanations
Gottesmann et al 1991
Johnson et al 1997
What did Gottesmann et al 1991 find
found a higher concordance rate for SZ among MZ twins (48%)
MZ share 100% of their DNA
Therefore the increase in concordance rate amongst MZ twins demonstrates that there is a genetic element to schizophrenia
What did Johnson et al 1997 find
conducted research on 3 Swedish triplets who all had SZ and found a genetic abnormality on the 15p gene
What is SZ considered as
Polygenic caused by many genes
what are 3 evaluation points of the Genetic explanation
- hard to separate genetic from environ as MZ are same sex, same house, same experiences so share both genetic and enviro
- Not 100% concordance rate + another factor (The diathesis stress model)
- support for polygenic - Ripke et al 2014 found evidence suggesting 108 genetic variations were associated with SZ including genes which code for dopamine
Explain the dopamine hypothesis AO1
Neurotransmitter
Hyperdopaminergia
hypodopaminergia
Abnormal levels of dopamine in both of these areas cause the symptoms of SZ unlike the original version of the dopamine hypothesis which said too much dopamine is the cause of SZ
Explain Hyperdopaminergia
High levels in the sub cortex causes speech poverty and auditory hallucinations
Explain hypodopaminergia
Low levels in prefrontal cortex is believed to be the cause of negative symptoms of SZ
What are three points to support the role of dopamine in the development of SZ
Antipsychotic drugs
Curran et al 2004
lindstroem et al 1999
Why does Antipsychotic drugs support the role of dopamine in the development of SZ
works to reduce dopamine in the brain is effective in reducing positive symptoms in 60% of cases if changing the level of dopamine reduces symptoms then is shows that dopamine does play a role
Why does Curran et al support the role of dopamine in the development of SZ
Reported that when a person who does not have SZ takes amphetamine (increases dopamine) start experiencing SZ symptoms and someone with SZ has a worse reaction
Why does Lindstroem et al 1999 support the role of dopamine in the development of SZ
Reported that chemicals responsible for the production of dopamine are taken up faster in the brains of SZ patients leading to increased levels of dopamine
give 2 AO3 points which don’t support the dopamine hypothesis
Antipsychotic drugs - 40% symptoms did not improve if high levels of dopamine were the only cause of SZ then it would be 100% effective
low research into low levels of dopamine in the cortex cause negative symptoms
Explain neural correlates with three key phrases
brain activity linked with symptoms
Avolition + ventral striatum
Hallucinations + superior temporal gyrus
Explain the phrase brain activity linked with symptoms in regard to neural correlates
Neural correlates are measurements of the structure of function of the brain that correlate with the + or - symptoms of SZ
Explain the phrase Avolition + ventral striatum in regard to neural correlates and use a study
Ventral striatum is involved in anticipation of reward(related to motivation)
Loss of motivation ( avolition) in SZ may be explained by low activity levels here
Juckel found a - correlation between Ventral striatum activity and overall - symptoms
Explain the phrase Hallucinations + superior temporal gyrus in regard to neural correlates using a study
Allen et al (2007) found that patients experiencing auditory hallucinations recorded lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus
Give a limitation of neural correlates
correlation - causation as is remains in question whether it is unusual activity in the brain causes symptoms or if there are other possible explanations for the correlation
Explain further correlation-nauseation as a limitation of neural correlates
A - correlation ay suggest that low activity in the ventral striatum causes avolition but it could be that avolition means that less info passes through the striatum resulting in the low activity.
Therefore although neural correlates exits it tells us little about the causes of SZ
