Biological Explanations For Schizophrenia Flashcards
Family studies- genetics
Family studies confirmed that genetic similarity aligns with vulnerability to the development of schizophrenia
Gottesman large scale family study- mz twins 48% concordance rate dz twins 17% 9% siblings
Most family’s share an environment so this is a correlation of both factors (diathesis stress model)
Candidate genes
Early research looked for a single gene that directly correlates with schizophrenia however researcher found that there are a number of candidate genes involved because sz is polygenic. The most likely genes would be those coding for neurotransmitters such as the COMT gene which codes for dopamine.
Schizophrenia is aetiologically heterogenous meaning that different combinations of genes can be involved such as genetic variation.
Mutation
Can have genetic variation in the absence of a family history of schizophrenia
Mutation in parental dna caused by radiation poison or viral infection can cause sz
Positive correlations fund between paternal age and risk of sz 0.7% in fathers at 20 2% in fathers over 50 as increase in age is associated with risk of sperm mutation.
Original dopamine hypothesis
Based on the discovery that antipsychotics which reduced DA levels caused symptoms similar to people with Parkinson’s disease which is associated with low da meaning sz must be associated with high levels of dopamine- hyperdopaminergia in sub cortical areas of the brain eg high levels of DA in the Broca’s area may explain speech poverty (negative symptom of SZ)
Revised dopamine hypothesis
Proposed addition of hypodopaminergia which is abnormally low levels of dopamine in the brains cortex eg low DA in the prefrontal cortex associated with complex thinking may explain negative symptoms which involve cognitive thinking like avolition.
It has also been suggested that subcortical hyperdopaminergia leads to cortical hypodopaminergia.
Genetics and early experiences of psychological or physical stress lead to subcortical hyperdopaminergia and therefore cortical hypodopaminergia.
Evaluation (strength)
+ strong evidence base, gottesman and tienari (adopted twin studies, if parents had SZ were still more likely to develop even though raised in a different environment)
+ evidence for dopamine hypothesis amphetamines increase DA levels and induce symptoms in people without the disorder and worsen symptoms in people with
Some candidate genes such as COMT gene acct on production of DA or DA receptors
Evaluation (weakness)
- diathesis stress model there is clear evidence that environmental factors also increase vulnerability to Sz so this approach lacks validity as it is biologically reductionist.
Childhood trauma- study showing 67% of people with SZ had at least one form of childhood trauma
Smoking cannabis associated with Schizophrenia - evidence for a central role of glutamate post-mortem and live scanning have found consistent high levels of glutamate in brain regions of people with Sz.