What are the two biological explanations for schizophrenia?
Genetic
Neural
how does schizophrenia run in families through genes?
heredity
Risk of developing disorder with schizophrenic family members is higher than for those who don’t have schizophrenic relatives
Different combinations of genes make individuals more vulnerable to schizophrenia
does having the genes for schizophrenia mean that an individual will inevitably develop schizophrenia?
No
Diathesis stress- environmental stressor might need to be contributed
what did Gottesman find in his study?
children with two schizophrenic parents- concordance rate 46%
Children with one schizophrenic parent- concordance rate 13%
children with schizophrenic siblings- concordance rate 9%
What were the findings of Joseph’s twin studies? What could we conclude from this?
concordance of DZ twins 7.4%
Concordance rate of MZ twins 40.4%
proves there is greater similarities due to genetic factors
How can you analyse concordance effectively?
rear twins apart from each other
Blind twin studies where the researcher doesn’t know the twin they are assessing is MZ or DZ
What is meant by the term neural correlates?
Changes in neuronal mechanisms resulting in the characteristic symptoms of schizmophrenia
how do different areas of the brain provide evidence for schizophrenia?
hippocampus- anatomical changes in the hippocampus of schizophrenic patients- Gotto and Grace- showed hippocampus dysfunction can influence levels of dopamine release
pre-frontal cortex- impaired in schizophrenic patients
grey matter- schizophrenic patients have a reduced volume of grey matter.
those displaying negative symptoms have enlarged ventricles- consequence of nearby parts not developing properly
white matter- reduced mylenation of white matter in schizophrenic patients
AO3 for neural correlates?
😊support for impact of grey matter deficits- Vita et al- patients with schizophrenia showed a higher reduction in cortical grey matter
😊implications for treatment-Addington et al- use of neuroimaging to predict those who will develop psychoses for earlier treatment
What are adoption studies?
Studies of genetically related individuals who have been reared apart
why are adoption studies useful in biological explanations? describe an example of an adoption study
adoption studies are used to study genetically related individuals reared apart, in order to distinguish between genetic and environmental influences
Tienari et al-164 adoptees whose bio mother was diagnosed with schizophrenia
6.7% also schizophrenic
compared to only 2% of 197 control adoptees who were born to non schizophrenic mothers
genetic liability to schizophrenia confirmed
describe what is meant by the dopamine hypothesis and explain the key ideas of the theory?
An excess of the neurotransmitter dopamine in certain brain regions is associated with positive symptoms of schizophrenia
neurones fire too easily or too often
Lead to hallucinations and delusions
abnormally high numbers of D2 receptors on receiving neurones, so more dopamine binds and more neurones fire
state evidence for the dopamine hypothesis concerning drugs that increase dopamine activity
amphetamine- dopamine agonist, stimulates nerve cells containing dopamine, causing the synapse to be flooded with dopamine
normal people who recieve large doses of amphetamine can develop characteristic delusions and hallucinations of schizophrenics
People suffering from parkinsons disease take the drug to raise dopamine levels and have been found to have schizophrenic type symptoms (Grilly)
State evidence for the dopamine hypothesis for drugs that decrease dapaminergic activity
Antipsychotic drugs
Block the activity of dopamine in the brain
Reduces activity in the neural pathways of the brain that use dopamine
Consequently these drugs eliminate hallucinations and delusions
These drugs are known as dopamine antagonists as they block the action of dopamine
Supports the role of dopamine in schizophrenia as the drugs used to reduce dopamine alleviates symptoms
what is the main principle of the revised dopamine hypothesis?
Davis and Khan proposed the positive symptoms of schizophrenia are caused by an EXCESS of dopamine in subcortical areas of the brain, particularly the mesolimbic pathway
Negative and cognitive symptoms thought to arise from a DEFICIT of dopamime in areas of the prefrontal cortex
two pieces of evidence to support the revised dopamine hypothesis?
neural imaging- Patel et Al used PET scans to assess dopamine levels, they were lower in the prefrontal cortex of schizophrenic patients compared to controls
Animal studies- wang and deutch- induced dopamine depletion on the prefrontal cortex in rats, resulted in cognitive impairment which could be reversed using antipsychotics, thought to have a beneficial effect on negative symptoms
evaluate genetic explanations for schizophrenia
☹️ rearing patterns may explain why schiz runs in families, instead of heredity- research on expressed emotion shows successive negative emotional climates in families can lead to stress, triggering a schizophrenic episode
☹️ MZ twins encounter more similar environments-research shows that greater concordance between MZ twins is a result of greater genetic similarity, but Joseph argues that MZ twins have a more similar environment that DZ twins, (eg- MZ= same sex) so treated more equally, differences in concordance between MZ and DZ twins may be therefore due to environment
evaluation of the dopamine hypothesis? (neural correlates)
😊evidence from treatment- antipsychotic drugs- alleviate schizophrenic symptoms. leutch et Al conducted meta analysis of 212 studies and found antipsychotics are significantly more effective compared to placebo
☹️Challenges to dopamine hypothesis- Noll claims that antipsychotic drugs don’t alleviate symptoms in about 1/3 of people, symptoms persist despite dopamine levels being normal, blocking D2 receptors dont do anything, so must be other neurotransmitter systems responsible for schizophrenia