711873
Description
Mind Map by Stephanie Bates, updated more than 1 year ago
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Created by Stephanie Bates
over 10 years ago
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Biological
Explanations for
SZ
- GENETIC EXPLANATIONS
- Genome scanning - 100s genes implicated.
Advances - type 3 dopamine receptor gene
(DRD3), type 2A serotonin receptor (HTR2A)
- SZ run in families, controlled genetic studies -
risk developing SZ inc/s w/ degree of genetic
relatedness. Twin studies - conc/ rate higher
MZs/DZs. Gottesman (1991) review studies
since 1966 - conc/ rate MZs - 50%, DZs (children
1 affected parent) - 17%. Gen/ Pop? - 1%
- MZs - not 100%. Other
factors (environment)
- MZs rare in population - of these 1%
expected SZ. Sample sizes small.
Cautious drawing conclusions.
- 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%
- Adoption studies
- Disentangle genetics / environmental
factors - born to SZ parents, brought by
ppl w/ no history of D
- 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.
- Not complete explanation
- Not complete explanation
- 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.
- Disentangle genetics / environmental
factors - born to SZ parents, brought by
ppl w/ no history of D
- Genome scanning - 100s genes implicated.
Advances - type 3 dopamine receptor gene
(DRD3), type 2A serotonin receptor (HTR2A)
- BIOCHEMICAL EXPLANATIONS
- Dopamine - neurotransmitter, limbic centre of brain.
- Dop/ Hypothesis - SZ
- excess dop/ activity
at certain synaptic
sites caused by:
- Release excess dop/ by presynaptic neurons
- Excess dop/ on receiving neurons = more dop/
binding to receptors = more neurons firing.
- Oversensitivity in dop/ recep/s
- Release excess dop/ by presynaptic neurons
- 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.
- Antipsychotic drugs (dop/ antagonists e.g.
phenothiazines) reduce symptoms. Block
activity of dop/ - reduceing stimulation of
dop/ system. Effectiveness = dop/
imbalance = sig/ contributory factor.
- Post-Mortems - inc/ dop/ in
left amygdala. Seeman
(1987) - reviewed studies -
inc/ dop/ receptor density,
60-100% / control groups.
- Not all benefit
phenothiazines - pos/
symptoms not neg/.
Diff/ types SZ - Diff/
causes. Clozapine -
oneof most clinically
effective - bind dop/ +
serotonin receptors.
Serotonin imp/.
- Post-Mortem - neuroleptic
drugs. Inc/ dop/ = drugs? SZ?
- Cause + Effect - correlated. dop/ = SZ or
SZ = excess dop/, receptors more
responsive. May be unknown variable.
- Dopamine - neurotransmitter, limbic centre of brain.
- Interaction - biol/+environment. Diathesis stress model - genetic vulnerability = physiological
weakness (dop/ sys/). =process info abnormally. + disrupted fam/ communications
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