Biological explanation of schizophrenia Flashcards

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1
Q

what have family studies shown about schizophrenia

A

that the risk of developing schizophrenia increases in line with genetic similarity to a relative with the disorder

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2
Q

what are the findings from Gottesman’s (1991) large-scale family study

A

risk of developing schizophrenia rises with genetic similarity:
monozygotic twins 48%
dizygotic twins 17%
siblings 9%
parents 6%

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3
Q

are candidate genes involved in schizophrenia

A

early research believed one faulty gene could explain schizophrenia, however it is impossible to pinpoint one specific gene responsible for schizophrenia
it is a polygenic condition, meaning many different candidate genes combine to cause schizophrenia

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4
Q

how many genetic variations are correlated with schizophrenia

A

Ripke et al (2014) found 108 separate genetic variations were associated with slightly increased risk of schizophrenia
as different studies have identified different candidate genes it appears schizophrenia is aetiologically heterogeneous

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5
Q

how are neural correlates related to schizophrenia

A

research has identified some neural correlates that can cause the symptoms of schizophrenia, for example brain structure or function

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6
Q

what is the most prevalent neural correlate of schizophrenia

A

the neurotransmitter dopamine (DA), it is important in the functioning of several brain systems related to the symptoms of schizophrenia

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7
Q

what did Kenneth Davis et al (1991) propose

A

the addition of cortical hypodopaminergia, for example, abnormally low DA in the brain’s cortex. this could explain cognitive problems like negative symptoms of schizophrenia

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8
Q

what can cortical hypodopaminergia lead to

A

subcortical hyperdopaminergia, where both high and low levels of DA in different brain regions are part of the updated dopamine hypothesis

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9
Q

what can make people more sensitive to cortical hypodopaminergia and subcortical hyperdopaminergia

A

current versions of the dopamine hypothesis try to explain the origins of abnormal DA levels and symptoms.
both genetic variations and early experiences of stress, both psychological and phyiscal (Howes et al 2017)

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10
Q

what is the evidence of research support of the genetic explanation (strength)

A

family studies such as Gottesman show that risk increases with genetic similarity
adoption studies such as Tienari et al (2004) show that biological children of parents with schizophrenia are at a heightened risk even if they grow up in an adoptive family

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11
Q

what is the evidence to show that environmental factors also increase the risk of developing schizophrenia (limitation)

A

environmental factors includes biological influences such as birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al 2015)
also psychological risk factors such as childhood trauma which leaves people vulnerable to mental health problems - Morkved et al (2017) found 67% of people with schizophrenia reported at least one childhood trauma

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11
Q

how can the role of genes in schizophrenia be applied to genetic counselling (discussion)

A

if one or more potential parents have a relative with schizophrenia, they risk having a child who could develop the condition
however the risk estimate is just an average figure and will not really reflect the likelihood of a particular child developing schizophrenia as they will experience different environments which has risk factors

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12
Q

what evidence is there for dopamine (strength)

A

antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher et al 2014)
some candidate genes act on the production of DA or DA receptors
this strongly suggests that dopamine is involved in the symptoms of schizophrenia

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13
Q

what is the evidence for a central role of glutamate (limitation)

A

post-mortem and live scanning studies have found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon et al 2020)
in addition, several candidate genes are believed to be involved in glutamate production or processing
this means an equally strong case can be made for the role of other neurotransmitters

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