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
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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)
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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
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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
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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
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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
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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
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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
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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
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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
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