Biological Explanations for Schizophrenia

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Genetic Basis - Gottesman's family study
Found MZ twins have a 48% shared risk of SZ, DZ twins have a 17% shared risk
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Polygenic and Aetiologically heterogeneous (inc. Ripke et al)
Existence of different candidate genes, different combinations can lead to Sz. Ripke studied 37,000 patients and found nearly 108 separate genetic variations associated with increased risk
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The dopamine hypothesis
Claims that an excess of dopamine in certain regions of the brain is associated with + symptoms of Sz
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D2 receptors
Those with Sz are thought to have an abnormally high number of D2 receptors on the receiving neurons, resulting in more dopamine bindings and neurons firing
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Hyperdopaminergia - subcortext and nucleus accumbens
High dopamine activity in the subcortex and nucleus accumbens associated with hallucinations (+ symptoms) and poverty of speech
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Hyperdopaminergia - Prefrontal Cortex
Low levels in the prefrontal cortex leads to negative symptoms
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Mesocorticalimbic system
Mesocortical Pathway Dysfunction = low levels of dopamine leads to negative symptoms, high dopamine leads to over-activity of the mesolimbic pathway, associated with + symptoms
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Neural Correlates features
Brain structure, ventricular enlargement, cellular disarray in the hippocampus, cerebral cortex reduced
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What are neural correlates?
Measurements of the structure or function of the brain that correlate with + or - symptoms of Sz
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Ventral Striatum (inc Juckel et al)
Involved in anticipation of reward (related to loss of motivation) as could be related to low activity here. Found a negative correlation between ventral striatum activity and overall negative symptoms
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Susser's research
flu during 1st trimester increases risk of Sz by 700%, 3rd trimester risk is 300%
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A03 SR Tienari et al
Out of 164 adopted children whose mothers had been diagnosed with Sz, 6.7% of children shared the diagnosis compared to 2% of 197 children with non-Sz mothers. Shows the effects of just genetics
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A03 Application to drugs Leucht et al
carried out a meta-analysis of 212 studies that had effectiveness of different antipsychotic drugs compared to a placebo. all were effective as they normalised dopamine levels
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A03 Johnstone et al
people with Sz had enlarged ventricles in their brain compared to those without Sz. Suggests that reduced volume of frontal and temporal lobe is linked to Sz
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A03 Suddath et al
Used MRI scans to obtain images of brain structure from MZ twins in which only one had Sz. the twin with Sz had enlarged ventricles than the twin without
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A03 environmental involvement
Concordance rates not 100% therefore must not be the sole explanation.
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Card 2

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Polygenic and Aetiologically heterogeneous (inc. Ripke et al)

Back

Existence of different candidate genes, different combinations can lead to Sz. Ripke studied 37,000 patients and found nearly 108 separate genetic variations associated with increased risk

Card 3

Front

The dopamine hypothesis

Back

Preview of the front of card 3

Card 4

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D2 receptors

Back

Preview of the front of card 4

Card 5

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Hyperdopaminergia - subcortext and nucleus accumbens

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