biological explanations

    Cards (9)

    • genetic basis - family studies
      the risk of schizophrenia increases in line with genetics - Gottesmans (1991) large scale family study:
      identical twin shares 100% of genes and 48% risk
      parents share 50% of genes and has 6% risk
      family members tend to share aspects of their environment so correlation shows both
    • genetic basis - candidate genes
      looked for a single genetic variation on the belief that one faulty gene could explain it - Ripke et al(2014) meta analysis of genetic studies:
      found 180 genetic variations of 37,000 sz compared to 113,000 controls
      schizophrenia is ateiologically heterogenous , different combinations of factors including genetic variations can lead to the condition
    • genetic basis - the role of mutation
      a genetic origin in the absence of a family history of the disorder
      mutation in parental DNA which can be caused by radiation, poison or viral infection
      Brown et al(2002) - age of father can increase risk of sz:
      0.7% under 25
      2% over 50
    • genetic basis evaluation strengths
      strong evidence from adoption studies - Tienari(2004):
      showed that the biological children of parents with sz are more high risk even if they grow up in adoptive families which rules out environmental factors
    • genetic basis evaluation limitations
      clear evidenc that there can be environmental factors aswell such as smoking cannabis
    • neural correlates - original dopamine hypothesis
      antipsychotic drugs used to treat sz (reduce dopamine) caused symptoms similar to parkinsons(low dopamine)- Seeman(1987)
      schizophrenia may be a high level of dopamine (hyperdopaminergia) in subcortal areas of the brain
      high dopamine in brocas area, may explain speech poverty and auditory hallucinations
    • neural correlates - updated dopamine hypothesis
      Davis (1991) - hypodopamergia (low dopamine) in the prefrontal cortex is responsible for negative symptoms of sz
      cortical hypodopaminergia leads to subcortical hyperdopaminergia
      high and low levels of dopamine in different brain regions part of the updated version
      diathesis stress model - predisposition that someone is vulnerable to sz is then brought about by a triggering event
    • neural correlates evaluation strengths
      support for the idea that dopamine is involved - (Curran 2004): amphetamines increase DA and worsen symptoms in people with sz and induce symptoms in people without
    • neural correlates evaluation limitations
      evidence for a central role of glutamate - (McCutcheon 2020): post-mortem and live scanning studies hvae consistently dound raised levels of the neurotransmitter glutamate in several brain regions of people with sz