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Evaluate the view that sz has a stronger bio basis than no bio (BIO;…
Evaluate the view that sz has a stronger bio basis than no bio
BIO; NeuroTransmitter
Dopamine Hypothsis
Excess dopamine receptors at the synapses cause SZ. + Drugs to increase dopamine production in Parkinson patients give psychotic symptoms. + genes linked with dopamine production are more frequent in SZ patients. + Anphetamines produce similar symptoms to those of excess dopamine. + Excess dopamine has a stimulant effect. + Increase of dopamine in Mesolimbic pathway creates positive symptoms and increase of Mesocotrical pathway creates negative symptoms. - PET scans show that blocking dopamine receptors doesn't always remove symptoms. - Glutamate could be impliacted. - Social and environmental factors are involved. - Different types of dopamine recptors in different areas give different results.
Glutamate Hypothesis
Glutamate Hypothesis; Suggests that the Lack of glutamate (HYPOGLUTAMATERGIA) didn't always lead to an increase in dopamine and if NMDA antagnosit (blocks receptor site) cause psychotic like symptoms the dopamine hypothesis was wrong. + Works with the dopamine hypothesis and expands on it. + Lots of evidence to support it (animal studies). - PET SCANS lack validity and can be seen as intrusive. -Animal studies lack generalisiability to humans
NON-BIO; Cognitive Models
Frith's Model
Suggests that people with SZ can't distinguish between actions driven by external forces and those by internal intention. Conscious processing is where the highest level of cognitive functioning takes place with awareness. Preconscious occurs without awareness and is automatic. If the filter between the two breaks down the unnecessary info will go to the conscious.This is how delusions are experienced as important info is misinterpreted. Down to a faulty filter, found in the pre-frontal cortex. +Acknowledges the bio approach plays a part. (diathesis stress model).
Helmley's model
Believes some psychotic symptoms arise from disconnection between stored knowledge and current sensory input. Stored knowledge = Schemas. In people with SZ the differentiation between schemas and new situations doesn't occur, they don't know which stimuli to ignore and which to attend. This is believed to be caused by abnormalities in hippocampus.
AO3; -Not universal support for Frith, fails to take in the environmental factors. +Treatment of CBT improves SZ symptoms suggesting changing faulty cognitions helps. + accounts for many of SZ positive symptoms, and the research into cognitive models is reliable and scientific making it credible. - It is not clear whether the cognitive dysfunction is a cause or effect of the disorder, building a theory on an observed correlation between thought processes and symptoms, but correlations do not prove cause. - The cognitive explanation by itself isn't a complete explanation. It could be said to DESCRIBE schizophrenia in more depth without really EXPLAINING where it comes from.
BIO; Genetics
ADOPTION; Heston 1947; followed 47 children born to a SZ mother but then adopted within 3 days of birth to families not associated with their biological ones. Later in life they were compared with a control group. 11% of the experimental group developed SZ compared to none in the control group. This separates the environmental from the biological.
C4 GENE; Sekar et al (2016); analysed 100,00 DNA samples of people with SZ from 30 different found C4 gene in the immune system. This gene plays a role in synapse pruning which happens during adolescence. Excess pruning causes SZ symptoms. Explains why SZ occurs after adolescence and why their brains cerebral cortex is thinner and they have fewer synapses.
TWIN STUDIES;Gottesman 1991; Looked at 40 different twin studies. He found that 48% of MZ twins both had SZ. DZ twins 17% both had SZ
FAMILY STUDIES; First degree relatives (Brother, sister, mother) share 50% of their genes. Second degree relatives (aunties, uncles, cousins) share 25% of their genes.Gottesman 1991; Found that SZ is more common in biological relatives with SZ. The closer the genetic link the greater the risk. If a brother or sister has SZ there is an 8% chance. If both your parents have SZ there is a 46% that you will get it.
TREATMENT
CBT
DRUGS