Biological explanation for Schizophrenia Flashcards
What chance do you have of developing SZ if your sibling has it? (Gottesman)
9%
What chance do you have of developing SZ if your MZ twins? (Gottesman)
48%
What chance do you have of developing SZ if your DZ twins? (Gottesman)
17%
What is polygenic, and what correlation does that have with SZ?
Polygenic = when there are a number of candidate genes which make up one disorder.
-> SZ is polygenic.
What is the most common neurotransmitter which codes for SZ?
Dopamine.
How many people did Ripke have in his sample who were diagnosed with SZ?
37,000
How many controls (without SZ) did Ripke have in his sample?
113,000
How many separate genetic variations were associated with an increased risk of SZ?
108 candidate genes.
What did the findings from Ripke’s study tell us about SZ?
It’s aetiologically heterogeneous.
What did Ripke’s study consist of?
He compared the genetic makeup of people with SZ to controls to find candidate genes with risk the onset of SZ.
What causes mutation in parents DNA?
Radiation, poison or viral infection.
What’s the risk of fathers with mutated sperm having kids who develop SZ according to Brown et al (2002)?
-0.7% in fathers under 25.
-2% in fathers over 50.
What is the best known neural correlate for SZ?
The neurotransmitter dopamine.
What was the original dopamine hypothesis based on?
Based on the discovery that drugs used to treat SZ caused symptoms similar to those in people with parkinson’s disease.
(Parkinsons = a condition associated with low DA levels).
What might SZ be a result of according to the original dopamine hypothesis?
High levels of DA (hyperdopaminergia) in the subcortical areas of the brain.
What part of the brain may explain specific symptoms like speech poverty/ auditory hallucinations?
Excess levels of DA receptors in pathway from the subcortex to Broca’s area.
What did David et al (1991) propose in the updated dopamine hypothesis?
The addition of cortical hypodopaminergia (abnormally low DA in the brains cortex).
What does the updated dopamine hypothesis tell us about SZ?
Cortical hypodopaminergia leads to subcortical hyperdopaminergia; so meaning both high and low levels of DA in different brain regions are part of the updates version (increase risk of SZ).
What does the neural explanation say about SZ according to Howes (2017)?
Both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia.
