biological explanations for schizophrenia Flashcards
1
Q
genetic basis of schizophrenia - family studies
A
- studies confirmed that risk of schizophrenia increases in line with genetic similarity to relatives with disorder (Irving Gottesman)
- family members tend to share aspects of environment as well as genes, correlation represents both
- family studies still give good support for importance of genes in schizophrenia
2
Q
genetic basis of schizophrenia - candidate genes
A
- early research looked for a single genetic variation, belief that one faulty gene could explain schizophrenia
- however, appears that number of different genes are involved
- most likely genes would be those coding for neurotransmitters, such as dopamine
- Stephen Ripke combined all previous data from genome-wide studies of schizophrenia
- genetic makeup of 37K people with schizophrenia was compared to 113K controls
- 108 separate genetic variations were associated with slightly increased risk of schizophrenia
- different studies have identified different candidate genes, so it appears tat schizophrenia is aetiologically heterogeneous (different combinations of factors, including genetic variation, can lead to the condition)
3
Q
genetic basis of schizophrenia - role of mutation
A
- schizophrenia can also have genetic origin in absence of family history
- one explanation for this is mutation in parental DNA which can be caused by radiation, poison or viral infection
- evidence for mutation comes from positive correlations between paternal age and risk of schizophrenia, increasing from 0.7% in fathers under 25 to 2% in fathers over 50
4
Q
neural correlates of schizophrenia
A
- we do not know exact cause of symptoms on biological level
- research has identified some neural correlates (brain structure or function etc.)
- best know neural correlate is dopamine (DA)
- important in functioning of several brain systems related to schizophrenia symptoms
5
Q
neural correlates of schizophrenia - original / historical dopamine hypothesis
A
- based on discovery that drugs used to treat schizophrenia caused symptoms similar to those in people with Parkinson’s, which is associated with low DA levels
- schizophrenia may therefore be result of high levels of DA in subcortical areas of the brain
- eg. excess of DA receptors in pathways from subcortex to Broca’s area may explain symptoms of schizophrenia such as poverty of speech
- abnormally high number of D2 receptors, resulting in more dopamine binding and therefore more neurons firing
- receptors may also be oversensitive
6
Q
neural correlates of schizophrenia - updated versions of dopamine hypothesis
A
- Kenneth Davis proposed addition of cortical hypodopaminergia (abnormally low DA in brain’s cortex)
- this can explain symptoms of schizophrenia
- eg. low DA in prefrontal cortex could explain cognitive problems
- also suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia, so both high and low levels of DA are part of updated version
- current versions of dopamine hypothesis also try to explain origins of abnormal DA function
- seems that both genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia
7
Q
evaluation strength for genetic basis - research support
A
- family studies show that risk increases with genetic similarity to family member with schizophrenia
- adoption studies show that biological children of parents with schizophrenia are at heightened risk even if they grow up in adoptive family
- recent twin study showed concordance rate of 33% for identical twins and 7% for non-identical twins
- some people more vulnerable to schizophrenia as result of genetic makeup
8
Q
evaluation limitation for genetic basis - environmental factors
A
- environmental factors include both biological and psychological influences
- study by Nina Morkved showed that 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma, compared to 38% of matched group with non-psychotic mental health issues
- genetic factors alone cannot provide complete explanation for schizophrenia
9
Q
evaluation strength for neural correlates - evidence for dopamine
A
- amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without
- antipsychotic drugs reduce DA activity and also reduce intensity of symptoms
- some candidate genes act on production of DA or DA receptors
- suggests that dopamine is involved in symptoms of schizophrenia
10
Q
evaluation limitation for neural correlates - glutamate
A
- evidence for central role of glutamate
- post-mortem and live scanning studies have found raised levels of neurotransmitter glutamate in brain regions of people with schizophrenia
- several candidate genes for schizophrenia believed to be involved in glutamate production or processing
- equally strong case can be made for role of other neurotransmitters