1.4 MZs rare in population - of these 1%
expected SZ. Sample sizes small.
Cautious drawing conclusions.
1.5 Diff/ distinguish MZs + DZs. Rigorous study - Cardno et al
(2002), Maudsley Twin Register, strict diagnostic criteria for
SZ + accurate zygosity assessment - MZs-26.5%, DZs-0%
1.6 Adoption studies
1.6.1 Disentangle genetics / environmental
factors - born to SZ parents, brought by
ppl w/ no history of D
126.96.36.199 Tienari (1991) - Finnish
Adoption Study - 155 adopt/d
child/ - biological mothers had
SZ. Compared to matched
group adopted children - no fam/
hist/ SZ. 10% mothers SZ
developed SZ, 1% 2nd Group.
188.8.131.52.1 Not complete explanation
2 BIOCHEMICAL EXPLANATIONS
2.1 Dopamine - neurotransmitter, limbic centre of brain.
2.2 Dop/ Hypothesis - SZ
- excess dop/ activity
at certain synaptic
sites caused by:
2.2.1 Release excess dop/ by presynaptic neurons
2.2.2 Excess dop/ on receiving neurons = more dop/
binding to receptors = more neurons firing.
2.2.3 Oversensitivity in dop/ recep/s
2.3 Dop/ neurons - key role in guiding
attention. Disturbances = probs w/
perception, attention + thought
characteristics of SZs (Comer, 2003).
Imbalance = inherited (genetic app/
(DRD3) or environment.
2.4 Antipsychotic drugs (dop/ antagonists e.g.
phenothiazines) reduce symptoms. Block
activity of dop/ - reduceing stimulation of
dop/ system. Effectiveness = dop/
imbalance = sig/ contributory factor.
2.5 Post-Mortems - inc/ dop/ in
left amygdala. Seeman
(1987) - reviewed studies -
inc/ dop/ receptor density,
60-100% / control groups.
2.6 Not all benefit
phenothiazines - pos/
symptoms not neg/.
Diff/ types SZ - Diff/
causes. Clozapine -
oneof most clinically
effective - bind dop/ +