Biological Explanations for Schizophrenia Flashcards
How do we investigate a genetic basis for schizophrenia?
Family, twin and adoption studies.
What did Gottesman’s findings show?
That genetics are not solely responsible for schizophrenia - if that was true then identical twins would have a 100% concordance rate, parents a 50%, and siblings a 25%.
Is Sz monogenic or polygenic?
Polygenic - there are up to 108 separate genes associated with it (Ripke).
What did Brown find about sperm mutation?
Older fathers had a 2% chance of fathering a child with schizophrenia due to their sperm mutating compared to a 0.7% chance from fathers under 25.
What is the evaluation - Tienari
Tienari found that adopted children with biological mothers who had Sz were more likely than controls to develop Sz, despite having non-schizophrenic adopted parents.
What is the evaluation - Hilker
Hilker did a twin study which found concordance rates of 33%. for MZ twins and 7% for DZ twins. This shows moderate gene influence but a much stronger environmental influence.
What is the evaluation - gene counselling?
If parents have got Sz then it increases the likelihood of their child developing it. Genetic counselling can be put in place to try to minimise risk factors which could prevent the onset of schizophrenia.
What is the evaluation - Birth complications, Cannabis use and trauma.
Morgan - Birth complications cause heightened chance of Sz development.
Di Forti - Smoking cannabis in teenage years also heightens risk.
Morkved - 67% of Sz patients report childhood trauma - 38% of general population.
What are 4 functions that dopamine plays a role in?
Pleasure/reward seeking behaviour.
Social Functioning
Movement
Cognition
What is the original dopamine hypothesis - Seeman?
Neurotransmitters function differently in a Sz brain. Dopamine has an excitatory effect, and unusually high levels are associated with positive symptoms. Messages from neurons that transmit dopamine fire too easily or too often in those with Sz, as they are thought to have abnormally high levels of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and more neurons finding.
What is the updated dopamine hypothesis - Davis?
Low levels of dopamine in the PFC lead to negative symptoms - avolition, speech poverty - HYPERDOPAMINERGIA.
High levels of dopamine in the sub cortex caused positive symptoms - overactive Broca’s area - hallucinations - HYPODOPAMINERGIA.
What is the evaluation - role of amphetamines?
Currant 2004 found that amphetamines increase dopamine, therefore increasing symptoms in schizophrenics and inducing schizophrenic symptoms in people without.
What is the evaluation - Tauscher
Antipsychotic drugs work to reduce dopamine activity and reduce intensity of symptoms therefore we know that dopamine is associated with production of certain symptoms
What is the evaluation - Ripke
Some of the 108 genes that Ripke found have been found to act on the production of DA or DA receptors.
What is the evaluation - Glutamate
McCutcheon found raised levels of glutamate in schizophrenics through post-mortems and brain scans. This is a limitation because an equally strong case can be made for the role of other neurotransmitters.
