schizophrenia ; biological explanations

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- genetic basis
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+ sz runs in families
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why is this quite weak evidence for a genetic link in itself?
family members share environment as well as genes
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but what is there a strong relationship between that we've seen from research?
degree of genetic similarity and shared risk of sz
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who was it that inv this?
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who found what % in MZ twins where one had sz tha the other would get it?
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and DZ?
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and parents?
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and siblings?
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but so why is the sibling / DZ this interesting?
same DNA split with siblings / DZ twins suggesting environment must have something to do with it too
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- candidate genes
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why does it appear sz is polygenic?
number of genes each appear to confer a small increased risk of sz
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why does it also appear that sz is aetiologically heterogeneous?
bc diff studies have identified different candidate genes
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what the **** does aetiologically heretogeneous mean?
different combinations can lead to the condition
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ripke et al carried out a huge study combining?
all prev data from genome-wide studies of sz
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genetic make up of how many patients used?
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compared to how many controls?
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how many separate genetic variations were associated with inc. risk of sz?
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genes associated w/ inc risk include coding for?
functioning of a number of neurotransmitters
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- the dopamine hypothesis
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+ neurotransmitters
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which chemical messenger in particular is widely believed to be involved?
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dopamine is important in the functioning of?
several brain systems implicated in symptoms of SZ
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+ hyperdopaminergia in the subcortex
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original version of dopamine hypothesis focused on?
high levels or activity of dopamine in the subcortex
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for example an excess of dopamine receptors in broca's area may be associated with?
poverty of speech +/or auditory hallucinations
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- hypodopaminergia in the cortex
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goldman-rakic et al identified what for negative symptoms?
low levels of dopamine in the prefrontal cortex
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the prefrontal cortex is responsible for?
thinking and decision making
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it may be that both hyper/hypo are correct how?
both high and low levels in different brain regions responsible
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- neural correlates of sz
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what are neural correlates?
measurements of the structure / function of the brain that correlate w/ an experience
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+ neural correlates of negative symptoms
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what does avolition involve?
loss of motivation
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what does motivation involve anticipation of?
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brain areas like where are involved in this anticipation?
ventral striatum
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abnormality of areas like ventral striatum may be involved in?
development of avolition
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juckel et al measured activity levels in ventral striatum in sz and found?
lower levels of activity than ctrls
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also observed a negative correlation between?
ventral striatum activity levels / severity of overall negative symptoms
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therfore activity in the ventrial striatum is a?
neural correlate of neg symptoms
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+ neural correlates of positive symptoms
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allen et al scanned the brains of patients experiencing?
auditory hallucinations
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and compared them to control group while they identified what?
pre-recorded speech as theirs / others
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lower levels in which two areas were found in hallucination grp?
superior temporal gyrus / anterior cingulate gyrus
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and they also did what more than ctrl group?
made errors
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we can thus say what about reduced activity in these two areas?
neural correlate of auditory hallucination
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:) multiple sources of evidence for genetic susceptibility
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gottesman study clearly shows what?
how genetic similarity and sared risk of sz are closely related
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tienari's adoption study clearly shows what about children of sz sufferers?
still @ high risk even if adopted into famblys with no history of sz
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evidence from studies @ molecular level show what?
particular genetic variation significantly increase sz
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therefore overwhelming evidence for what idea?
genetic factors make some ppl morevulnerable to developing sz than others
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but this doesn't mean what?
sz is entirely genetic
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number of environmental factors associated but available ev suggests?
genetic susceptibility is v important
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:( mixed evidence for the dopamine hypothesis
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curran et al found what about dopamine agonists like amphetamines?
make sz worse and can produce sz-like symptoms in non sufferers
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on the other had antipsychotic drugs work by?
reducing dopamine activity
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both inds of drug do suggest what tho?
important role for dopamine in sz
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radioactive labelling studies have found what about chemicals needed to produce dopamine?
taken up faster in brains of sz sufferers than ctrls
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produce more dopamine
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also ev to sugg dopamine doesn't provide?
complete explanation
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some genes identified in the ripke et al study code for?
production of other neurotransmitters
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so it appears?
otherneurotransmitters are important factors as are dopamines
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much of attention in current research has shifted to role of neurotrans called?
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evidence for dopamine hypothesis can @ best be described as?
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:( correlation-causation problem
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neural correlates are useful for doing wht?
flagging up particular brain systems
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but most importantly leaves what question unanswered?
does the unusual activity cause the symptom or nah
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for example with the levels of activity in ventral striatum and neg symptom what may be true?
something wrong in ventral striatum is causing negative symptoms
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but what is just as possible?
neg symptoms themselves mean that less info passesthrough striatum resulting in reduced activity
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what is a third possibility?
another factor influences both
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existence of neural correlates therefore tells us?
little in itself
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:( role of mutation
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sz can take place in the absence of what history?
family history with disorder
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one explanation for this is?
mutation in parental DNA
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this can be caused by?
radiation / poison / viral infection
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evidence for role of mutation comes from a correlational study showing?
positive correlation between paternal age and risk of sz
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what % is it at with fathers under 25?
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and over 50?
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:( role of psych env is important but unclear
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there;s also evidence in sz supporting importance of what?
environmental factors
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including psychological ones like?
family functioning in childhood
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- genetic basis



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+ sz runs in families


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why is this quite weak evidence for a genetic link in itself?


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but what is there a strong relationship between that we've seen from research?


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