biological explanations for schizophrenia Flashcards
3 genetic basis’s of schizophrenia
- family studies
- candidate genes
- role of mutation
what have family studies confirmed
risk of schizophrenia increases due to genetic similarity with relative who has disorder
what is a disorder called that can be caused by 1+ gene
polygenic
describe findings of gottesman (1991) large scale family study
- general population = 1% risk of schizophrenia
- 6% risk if either parent has schizophrenia
- 17% dizygotic twins
- 48% monozygotic twins
what did gottesman & shield find
- children with 2 schizophrenic parents had concordance rate of 46%
- children with 1 schizophrenic parent had concordance rate of 13%
- siblings had concordance rate of 9%
adoption study findings by tienari et al. (2000)
- finland
- 164 adoptees
- found 11 (6.7%) received diagnosis if biological parent diagnosed
- compared to 4 (2%) of 197 control adoptees (non-schizophrenic mothers)
AO3 twin studies (-) identical twins treated more similar
E: loehlin & nichols (1976) argue identical twins treated more similar & spend more time together
T: may explain why MZ twins have higher concordance rates than DZ twins as environment more similar
describe candidate genes as a genetic explanation for schizophrenia
- many genes involved (polygenic)
- most likely genes = code for neurotransmitters eg. dopamine
- schizophrenia is aetiologically heterogeneous, as different studies have identified different candidate genes
define aetiologically heterogeneous
different combinations of factors (eg. genetic variation) can lead to condition
study by ripke et al. (2014) - candidate genes
- combined previous data from genome-wide studies (looks at whole genome, not just genes) of schizophrenia
- genetic make-up of 37,000 people with schizophrenia compared to 113,000 controls
- 108 separate genetic variations associated with increased risk
describe the role of mutation as a genetic explanation for schizophrenia
- schizophrenia can have genetic origin, even if absence in family history of disorder:
- mutation in parental DNA, caused by eg. radiation, poison, viral infection
evidence for role of mutations causing schizophrenia
brown et al. 2002
- positive correlations between paternal age (increased risk of sperm mutation) & risk of schizophrenia
- 0.7% in fathers under 25
- over 2% in fathers over 50
genetic explanation: AO3 (+) strong evidence to support
E:
- family studies (eg. gottesman) show risk increases with genetic similarity to family member with schizophrenia
- adoption studies (eg. tienari et al. 2004) showed biological children of parents with schizophrenia at heightened risk, even if grow up in adoptive family
- study by hilker et al. (2018) showed concordance rate of 33% for MZ twins & 7% for DZ twins
T: shows how some people more at risk to schizophrenia due to genetic make-up
genetic explanation AO3 (-) clear evidence to show environmental factors also increase risk of schizophrenia
E:
- biological & psychological influences
- biological factors eg. birth complications (morgan et al. 2017), smoking THC-rich cannabis during teens (di forti et al. 2015)
- psychological factors eg. childhood trauma (more vulnerable - morkved et al. 2017)
T: means genetic factors alone cannot provide complete explanation for schizophrenia
evidence for link between childhood trauma (psychological factor) & schizophrenia
morkved et al. (2017)
- 67% people with schizophrenia & related psychotic disorders reported minimum 1 childhood trauma
- compared to 38% of matched group with non-psychotic mental health issues
2 neural correlates of schizophrenia
- original dopamine hypothesis
- updated versions of dopamine hypothesis
describe the original dopamine hypothesis
- based on discovery that drugs used to treat schizophrenia (antipsychotic - reduce DA) cause symptoms similar to Parkinson’s disease (low DA) = seeman 1987
- schizophrenia result of high DA (hyperdopaminergia) in subcortical areas of brain eg. excess DA receptors in pathway from subcortex to Broca’s area = may explain symptoms eg. poverty of speech, auditory hallucinations
hyperdopaminergia
high dopamine levels
describe the updated dopamine hypothesis
- davis et al. (1991) proposed additional cortical hypodopaminergia (low levels)
- eg. low DA in prefrontal cortex may explain cognitive problems
- suggested that cortical hypodopaminergia can lead to subcortical hyperdopaminergia
- howes et al. (2017) genetic variations & early experiences of stress (psychological/physical) make some more sensitive to cortical hypodopaminergia & thus, subcortical hyperdopaminergia
hyperdopaminergia
abnormally low levels of dopamine in brains cortex
neural correlates AO3 (+) support for idea that dopamine is involved in schizophrenia
E:
- amphetamines increase DA & worsen symptoms in those with schizophrenia & induce symptoms in those without (curran et al. 2004)
- antipsychotic drugs reduce DA activity & reduce intensity of symptoms (tauscher et al. 2014)
- some candidate genes act on production of DA or DA receptors
T:
- suggests dopamine is involved in symptoms of schizophrenia
neural correlates AO3 (-) dopamine hypothesis contradicted by evidence for central role of glutamate
E:
- post-mortem & live scanning studies consistently found higher levels of glutamate in several regions in brain of people with schizophrenia (McCutcheon et al. 2020)
- several candidate genes for schizophrenia believed to be involved in glutamate production/processing (eg. ripke et al. 2014)
T: shows that there’s a strong case for role of other neurotransmitters & dopamine hypotheses cannot sufficiently explain schizophrenia
