biological explanations of schizophrenia

Question 1

Genetic basis

Answer 1

• Family studies
• Candidate genes
• Role of mutation

Question 2

Genetic basis: Family studies

Answer 2

• risk of schizophrenia increases in line with genetic similarity
• Gottesman (1991): carried out a large-scale family study
  
  • MZ twins have 48% concordance
  • DZ twins have 17% concordance
  • parent have a 6% concordance
• weak evidence for a genetic basis as family members also share the same / similar environment as well as genetics
• shows that more similar genes are within a family more likely a member of the family is likely to have schizophrenia

Question 3

Genetic basis: candidate genes

Answer 3

• number of genes increase the risk of a person getting schizophrenia
• schizophrenia is polygenic
• studies have found different candidate genes meaning that schizophrenia appears to be aetiologically heterogeneous
• Ripke et al (2014): carried out a huge study by combining previous data from genome-wide studies
  
  • genetic make-up of 37,000 patients were compared to that of 113,000 controls
  • 108 separate genetic variations were associated with the risk of schizophrenia
  • genes associated with the increased risk included those coding for the functioning of a number of neurotransmitters (dopamine)

Question 4

Genetic basis: role of mutation

Answer 4

• mutation in parental DNA caused by radiation, poison or viral infection
• evidence from positive correlations between paternal age (associated with increased risk of sperm mutation) & risk of schizophrenia
  
  • increases from 0.7% with fathers under 25 to over 2% in fathers over 50

Question 5

AO3 - genetic basis: research support

Answer 5

• strong evidence for the support of the genetic explanation
• Gottesman (1991): shows how genetic similarity & the shared risk of getting schizophrenia are related
• adoption studies such as Tienari et al (2004) show that children of schizophrenia sufferers are still at a heightened risk of schizophrenia
  
  • if adopted into families with no history of schizophrenia
• Ripke et al (2014): conducted studies on a molecular level & found that particular genetic variations significantly increase the risk of schizophrenia

Question 6

AO3 - genetic basis: environmental factors (W)

Answer 6

• biological risk factors: birth complications & smoking THC-rich cannabis in teen years
• psychological risk factors: childhood trauma leaves people more vulnerable adult mental health problems in general & there’s now more evidence for a particular link
• research shows that 67% of people with schizophrenia & related psychotic disorders reported at least one childhood trauma
• opposed to 38% of a matched group with non-psychotic mental health issues
• genetic factors alone cannot provide a complete explanation for schizophrenia

Question 7

AO3 - genetic basis: genetic counselling (S)

Answer 7

• one application of our understanding of the role of genetics in schizophrenia is genetic counselling
• if one / more potential parents have a relative with schizophrenia & they risk having a child with schizophrenia
• risk estimate is just an average figure & it won’t really reflect the probability of a particular child going on to develop schizophrenia as they will experience a particular environment which also has risk factors
• may not always be helpful as many may
  
  • treat the child differently
  • abort child as they aren’t as imagined

Question 8

Neural correlation

Answer 8

• refers to the brain structure or function of schizophrenia
• Original dopamine hypothesis
• Updated versions of the dopamine hypothesis

Question 9

neural correlation: original dopamine hypothesis

Answer 9

• based on the discovery that drugs used to treat to schizophrenia cause symptoms similar to those of Parkinson’s disease ( linked to low dopamine)
• concluded schizophrenia might be linked to high levels of dopamine (hyperdopaminergic in the subcortical areas of the brain)
• e.g: excess of dopamine receptors in Broca’s area may be associated with speech poverty or auditory hallucinations

Question 10

neural correlation: updated versions of the dopamine hypothesis

Answer 10

• recent versions have focused on abnormal dopamine systems in the brain’s cortex
• Goldman-Rakic et al (2004): identified a role for low levels of dopamine (hyperdopaminergic) in the prefrontal cortex in the negative symptoms of schizophrenia

Question 11

neural correlation - AO3: evidence for dopamine (S)

Answer 11

• support from a number of sources for abnormal dopamine
• dopamine agonists like amphetamine that increase levels of dopamine make schizophrenia worse & can produce schizophrenia-like symptoms in non-sufferers
• anti-psychotic drugs work by reducing dopamine activity which suggests its an important role for dopamine
• evidence to suggest that dopamine doesn’t provide a complete explanation for schizophrenia
• some genes have been identified in the Ripke study for the production of other neurotransmitters ( research is looking at glutamate)
• evidence for dopamine is mixed - may be both hyper & hyperdopaminergic as people are different

Question 12

neural correlation - AO3: glutamate (W)

Answer 12

• evidence for the role of glutamate
• live brain scans & post-mortems have consistently found raised levels of glutamate in several areas of the brain in those with schizophrenia
• several candidate genes are thought to be responsible for glutamate production or processing
• glutamate is equally important as the role of other neurotransmitters

Question 13

neural correlation - AO3: amphetamine psychosis (S)

Answer 13

• Tenn et al (2003): induced schizophrenia-like symptoms in rats using amphetamines & then reduced symptoms using drugs that reduce dopamine actions
  
  • supports dopamine hypothesis
• other drugs that increase dopamine don’t cause schizophrenia-like symptoms
• Garson (2017) challenged the idea that amphetamine psychosis closely mimics schizophrenia