biological explanations for schizophrenia

Question 1

what evidence was there for schizophrenia running in family

(GOTTESMAN)

Answer 1

schiz runs in families.
GOTTESMAN 1991 large scale family study:
1% whole pop
grandchildren 5%
parents 6%
siblings 9%
non-denticle 17%
identical 48%

Question 2

what’s a limitation of schizophrenia running in family

Answer 2

we share the same enviorment
as well

Question 3

what was Stephen Ripke et al study into candidate genes

Answer 3

huge study combining all previous data from genome-wide studies of schizophrenia.
genetic make up of 37000 patients was compared to 113000 controls; 108 separate genetic variations were associated w increased risk go schiz.
increased risk included coding of functioning neurotransmitters including dopamine.

Question 4

what was Stephens Ripke sample

Answer 4

37,000 schiz patients compared to 113,000 controls.

Question 5

dopamine hypothesis:
explain what the neurotransmitter effects

Answer 5

neurotransmitters, brains chemical messengers work differently w schiz patient. dopamine implicated in symptoms

Question 6

dopamine hypothesis:
explain the effect of hyperdopaminegia in the subcortext

Answer 6

orignal dopamine hypothesis focused on high levels or activity of dopamine in subcortext (central areas of brain).

Question 7

what’s the effect of excess dopamine receptors in Brocas area

Answer 7

poverty of speech and/or experiences of auditory halluinciations.

Question 8

what’s the hypodaminergia in the cortex

Answer 8

more recent version of dopamine hypothesis
focuses instead on abnormal dopamine systems in the brain cortex.

Question 9

what did Goldman-rakic et al find for hypodopaminergia in cortex

Answer 9

identified role for low levels of dopamine in the prefrontal (responsible for thinking & decision making) in negative symptoms of schiz.
it may be both hyper/hypod are correct explanations. both high n low levels of dopamine in different brain regions.

Question 10

what’s neural correlations mean and how is it linked to schiz

Answer 10

r measurement of structure or function of the brain that correlate with an experience.
schiz- both positive n negative symptoms have neural correlation.

Question 11

neural corrlates of negative symptoms

Answer 11

avolition = loss of motivation
motivation involves anticipation of a reward. VENTRAL STRIATUM involved w this anticipation.
abnormality of this area may be involved in development of avolition.
Juckel studied this

Question 12

what was Juckel et al study into ventral striatum

Answer 12

measured activity levels in ventral striatum in schiz n found lower activity levels than those in controls.
they observed a negative correlation between activity levels in the VS n the severity of overall negative symptoms.
THUS VS is neural correlate of negative symptoms.

Question 13

neural correlates of positive symptoms
(allen et al)

Answer 13

ALLEN scanned brains if patients experiencing auditory hallucinations compared to control group.
identified pre-recorded speech as theirs or others.
lower activation levels in superior temporal gyrus & anterior cingulate gyrus found in hallucination group, who also made more errors than control group.
= reduced activity in 2 areas is a neural correlate of auditory halluncations.

Question 14

evaluation of biological explanations
multiple sources of evidence for genetic susceptibility

Answer 14

strong evidence for genetic vulnerability.
Gottesman
adoption studies by Pekka Tienari - children of schiz sufferers still at heightened risk of developing schiz than others. even if adopted into fam w no history.

this all suggests that genetic factors make ppl much more vulnerable to developing schiz than others. genetic susceptibility is very important.

Question 15

A02
mixed evidence for dopamine hypothesis

Answer 15

number of support for abnormal dopamine functioning in schiz.

dopamine agonists like amphetamines that increase levels of dopamine make schiz worse & can produce shiz like symptoms in non-sufferers. (Curran et al).
antipsychotic drugs, work by reducing dopamine activity (tauscher et al)
both kind of drug studies suggest important role for dopamine in schiz.

radioactive labelling studies (Lindstroem et al) found chemicals needed to produce dopamine r taken up faster in brain of schiz sufferers than controls suggesting they produce more dopamine.

appears dopamine is an important factor in schiz so r other neurotransmitters. current research shifted to role of neurotransmitters - glutamate. evidence for dopamine hypothesis is described as mixed.

Question 16

A02
the correlation- causation problem

Answer 16

number of neural correlates w positive & negative symptoms. although useful leaves questions unanswered.
does the unusual activity in a region of the brain cause the symptom?
it may be something wrong in the striatum causing negative symptoms. or it may be possible that the negative symptoms themselves mean less information passes thru the striatum = reduced activity.

this means that the existence of neural correlates in schiz tells us little in itself.

Question 17

A02
role of mutation

Answer 17

schiz can take place in the absence of family history of the disorder.
parental sperm cells.
this can be caused by radiation, poison or viral infection.
evidence from study showing a positive correlation between parental age and risk of schiz, increasing 0.7% with fathers under 25 to over 2% in fathers over 50.

Question 18

what are all the A02 points for biological explanations for schiz

Answer 18

1. multiple sources of evidence for genetic susceptibility
2. mixed evidence for the dopamine hypothesis
3. the correlation-causation problem
4. the role of mutation