biological explanations for Sz Flashcards
what did Gottesman find about the relationship between genes and Sz
Sz is partly genetic, with ~50% concordance rates for genetically identical twins, with a positive correlation between the % of genes shared and the risk of developing Sz
what did Ripke do with candidate genes
combined research of genome-wide studies. he compared the genetic makeup of 37,000 with Sz to 113,000 controls without Sz (total of 150,000)
what did Ripke find
108 separate genes associated with a slightly increased risk of Sz
how is Sz attributed genetically
Polygenic
how can Sz occur in the absence of a family history of the disorder
Mutation in parental DNA, can be caused by radiation, poison, or viral infection.
seen by a positive correlation between paternal age (risk of sperm mutation) and risk of Sz, increasing from ~0.7% with fathers aged <25 to >2% in fathers aged >50
what’re 3 strengths of the genetic explanation for Sz
adoption studies
concordance rates in twin studies
genetic counselling
how are adoption studies a strength for genetic explanations for Sz
Tienari et al. found adopted children with biological mothers who had Sz were more likely than controls to develop Sz, even with non-Sz adopted parents
how are concordance rates from twin studies a strength of the genetic explanation for Sz
Hilker et al found concordance rates for Sz of 33% in MZ and 7% for DZ twins.
this shows that Sz does have genetic basis but with relatively low concordance rates
how is genetic counselling a support of genetic explanations for Sz
if parents have Sz, it increases the risk of development for their offspring. research has led to genetic counselling which can be used to try to minimise risk factors which could prevent the onset of Sz
what’re neural correlates
there are brain areas, structures or functions which appear related to Sz. in particular, dopamine (DA) has been found to be strongly associated with the illness
what’re functions that dopamine plays a role in
pleasure/reward seeking behaviour
social functioning
movement
cognition
what did Seeman find in the original dopamine hypothesis
- Sz patients’ neurotransmitters work differently
- dopamine is an excitatory neurotransmitter associated with pleasure
- unusually high levels are associated with Sz, positive symptoms in particular
- messages from neurons that transmit dopamine fire too easily/often in Sz patients
- Sz patients are thought to have abnormally high levels of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and neurons firing
what symptom is associated with high levels of dopamine
hyperdopaminergia, in the sub-cortical areas of the brain such as Broca’s area (can lead to auditory hallucinations)
what symptom is associated with low levels of dopamine
Hypodopaminergia, in the cortical area of the brain, eg the PFC
what is the updated dopamine hypothesis, by Davis
- high levels of dopamine aren’t found in all Sz patients, and the modern drug clozapine, wish very little DA-blocking activity, is effective against Sz.
- suggests that hypodopaminergia can also explain Sz but for negative symptoms
- therefore both too high/low levels of DA in different brain areas are associated with Sz symptoms
- It has also been suggested that Cortical hypodopaminergia can cause subcortical hyperdopaminergia