schizophrenia ; biological explanations

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BIOLOGICAL EXPLANATIONS
DFGHFGD
1 of 85
- genetic basis
dgd
2 of 85
+ sz runs in families
dfgdg
3 of 85
why is this quite weak evidence for a genetic link in itself?
family members share environment as well as genes
4 of 85
but what is there a strong relationship between that we've seen from research?
degree of genetic similarity and shared risk of sz
5 of 85
who was it that inv this?
gottsman
6 of 85
who found what % in MZ twins where one had sz tha the other would get it?
48%
7 of 85
and DZ?
17%
8 of 85
and parents?
6%
9 of 85
and siblings?
9%
10 of 85
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
11 of 85
- candidate genes
dfgd
12 of 85
why does it appear sz is polygenic?
number of genes each appear to confer a small increased risk of sz
13 of 85
why does it also appear that sz is aetiologically heterogeneous?
bc diff studies have identified different candidate genes
14 of 85
what the **** does aetiologically heretogeneous mean?
different combinations can lead to the condition
15 of 85
ripke et al carried out a huge study combining?
all prev data from genome-wide studies of sz
16 of 85
genetic make up of how many patients used?
37,000
17 of 85
compared to how many controls?
113,000
18 of 85
how many separate genetic variations were associated with inc. risk of sz?
108
19 of 85
genes associated w/ inc risk include coding for?
functioning of a number of neurotransmitters
20 of 85
including?
dopamine
21 of 85
- the dopamine hypothesis
dfgd
22 of 85
+ neurotransmitters
dfgdf
23 of 85
which chemical messenger in particular is widely believed to be involved?
dopamine
24 of 85
dopamine is important in the functioning of?
several brain systems implicated in symptoms of SZ
25 of 85
+ hyperdopaminergia in the subcortex
dfgd
26 of 85
original version of dopamine hypothesis focused on?
high levels or activity of dopamine in the subcortex
27 of 85
for example an excess of dopamine receptors in broca's area may be associated with?
poverty of speech +/or auditory hallucinations
28 of 85
- hypodopaminergia in the cortex
dfgd
29 of 85
goldman-rakic et al identified what for negative symptoms?
low levels of dopamine in the prefrontal cortex
30 of 85
the prefrontal cortex is responsible for?
thinking and decision making
31 of 85
it may be that both hyper/hypo are correct how?
both high and low levels in different brain regions responsible
32 of 85
- neural correlates of sz
dfgd
33 of 85
what are neural correlates?
measurements of the structure / function of the brain that correlate w/ an experience
34 of 85
+ neural correlates of negative symptoms
dfgd
35 of 85
what does avolition involve?
loss of motivation
36 of 85
what does motivation involve anticipation of?
reward
37 of 85
brain areas like where are involved in this anticipation?
ventral striatum
38 of 85
abnormality of areas like ventral striatum may be involved in?
development of avolition
39 of 85
juckel et al measured activity levels in ventral striatum in sz and found?
lower levels of activity than ctrls
40 of 85
also observed a negative correlation between?
ventral striatum activity levels / severity of overall negative symptoms
41 of 85
therfore activity in the ventrial striatum is a?
neural correlate of neg symptoms
42 of 85
+ neural correlates of positive symptoms
dfgd
43 of 85
allen et al scanned the brains of patients experiencing?
auditory hallucinations
44 of 85
and compared them to control group while they identified what?
pre-recorded speech as theirs / others
45 of 85
lower levels in which two areas were found in hallucination grp?
superior temporal gyrus / anterior cingulate gyrus
46 of 85
and they also did what more than ctrl group?
made errors
47 of 85
we can thus say what about reduced activity in these two areas?
neural correlate of auditory hallucination
48 of 85
EVALUATION
sdss
49 of 85
:) multiple sources of evidence for genetic susceptibility
dfgdf
50 of 85
gottesman study clearly shows what?
how genetic similarity and sared risk of sz are closely related
51 of 85
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
52 of 85
evidence from studies @ molecular level show what?
particular genetic variation significantly increase sz
53 of 85
therefore overwhelming evidence for what idea?
genetic factors make some ppl morevulnerable to developing sz than others
54 of 85
but this doesn't mean what?
sz is entirely genetic
55 of 85
number of environmental factors associated but available ev suggests?
genetic susceptibility is v important
56 of 85
:( mixed evidence for the dopamine hypothesis
dfgd
57 of 85
curran et al found what about dopamine agonists like amphetamines?
make sz worse and can produce sz-like symptoms in non sufferers
58 of 85
on the other had antipsychotic drugs work by?
reducing dopamine activity
59 of 85
both inds of drug do suggest what tho?
important role for dopamine in sz
60 of 85
radioactive labelling studies have found what about chemicals needed to produce dopamine?
taken up faster in brains of sz sufferers than ctrls
61 of 85
suggesting?
produce more dopamine
62 of 85
also ev to sugg dopamine doesn't provide?
complete explanation
63 of 85
some genes identified in the ripke et al study code for?
production of other neurotransmitters
64 of 85
so it appears?
otherneurotransmitters are important factors as are dopamines
65 of 85
much of attention in current research has shifted to role of neurotrans called?
glutamate
66 of 85
evidence for dopamine hypothesis can @ best be described as?
mixed
67 of 85
:( correlation-causation problem
dfg
68 of 85
neural correlates are useful for doing wht?
flagging up particular brain systems
69 of 85
but most importantly leaves what question unanswered?
does the unusual activity cause the symptom or nah
70 of 85
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
71 of 85
but what is just as possible?
neg symptoms themselves mean that less info passesthrough striatum resulting in reduced activity
72 of 85
what is a third possibility?
another factor influences both
73 of 85
existence of neural correlates therefore tells us?
little in itself
74 of 85
EVAL EXTRA
DFGDF
75 of 85
:( role of mutation
dfgdf
76 of 85
sz can take place in the absence of what history?
family history with disorder
77 of 85
one explanation for this is?
mutation in parental DNA
78 of 85
this can be caused by?
radiation / poison / viral infection
79 of 85
evidence for role of mutation comes from a correlational study showing?
positive correlation between paternal age and risk of sz
80 of 85
what % is it at with fathers under 25?
0.7%
81 of 85
and over 50?
2%
82 of 85
:( role of psych env is important but unclear
dhdf
83 of 85
there;s also evidence in sz supporting importance of what?
environmental factors
84 of 85
including psychological ones like?
family functioning in childhood
85 of 85

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Card 2

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- genetic basis

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dgd

Card 3

Front

+ sz runs in families

Back

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Card 4

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

Back

Preview of the front of card 4

Card 5

Front

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

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