Biological explanation for Schizophrenia

Question 1

who did the large scale family study

Answer 1

Irving Gottesman (1991)

Question 2

what are the percentages that Gottersman (1991) found

Answer 2

48% for identical twins
17% for fraternal twins
6% for siblings

Question 3

what does aetiologically hetrogenoues mean

Answer 3

• different combinations of factors can lead to the condition

Question 4

what does polygenic mean

Answer 4

• multiple different genes are involved in schizophrenia

Question 5

who studied candidate genes for schizophrenia

Answer 5

Ripke et al (2014)

Question 6

how did Rikpe et al (2014) study candidate genes for schizophrenia

Answer 6

• combined all previous data from genome wide studies of schizophrenia
• genetic make up of 37,000 people with schizophrenia was compared to 113,000 controls
• identified 108 separate genetic variations associated with increased risk of schizophrenia

Question 7

what neurotransmitter is associated with schizophrenia

Answer 7

dopamine

Question 8

strength of genetic explanation

Answer 8

1. Research support
   - Family studies such as Gottersman show that risk increased with genetic similarity to family members with Schizophrenia
   - adoption studies by Tieneri et al (2004) showed that biological children of parents with schizophrenia are at a heightened risk even if they grow up in an adoptive family
   - Hilker er al twin study showed a concordance rate of 33% for identical twins and 7% for non identical twins

Question 9

limitation of the genetic explanation

Answer 9

1. environmental factors
   - biological risk factors - birth complications (Morgan et al 2017), smoking THC rich cannabis in teenage years (Di Forti et al 2015)
   - psychological risk factors - childhood trauma which leaves people more vulnerable to adult mental health problems
   - study by Morkved et al (2017) found that 67% of people of schizophrenia reported at least 1 childhood trauma as opposed to 38% of a matched group with non psychotic mental health issue

Question 10

what is the original dopamine hypothesis

Answer 10

• based on the discovery that drugs used to treat schizophrenia caused symptoms similar to those with people with Parkinson’s disease, a condition associated with low dopamine levels
• so schizophrenia must be a result of high levels of DA (hyperdopaminergia) in subcortical areas of the brains
• excess DA receptors in the pathways from the subcortex to Broca areas may explain specific symptoms of schizophrenia such as speech poverty and auditory hallucinations

Question 11

who proposed the updated versions of the dopamine hypothesis

Answer 11

Davis et al (1991)

Question 12

what is the updated version of the dopamine hypothesis

Answer 12

• addition of hypodopaminergia (Abnormal low DA in the brain cortex)
• low DA in the prefrontal cortex could explain cognitive problems (negative symptoms)
• cortical hypodppaminergia leads to subcortical hyperdopaminergia
• both genetic variation and early experiences of stress make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia

Question 13

strength of the dopamine hypothesis

Answer 13

1. evidence for dopamine
   - amphetamines increased DA and worsens symptoms in people with schizophrenia and induces symptoms in people without (Curren et al 2004)
   - antipsychotic drugs reduce DA activity and reduce the intensity of symptoms (Tauscher et al 2014)
   - some candidate genes act on the production of DA or its receptors

Question 14

limitation of dopamine hypothesis

Answer 14

1. glutamate
   - evidence for a central role of glutamate
   - post mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon et al 2020)
   - several candidate genes for schizophrenia are believed to be involved in glutamate production or processing