Biological explanations

• What is the genetic explanation for schizophrenia (SZ)?

  Genetic predisposition increases SZ probability
• What did Gottesman (1991) find regarding family studies and SZ?

  Higher genetic similarity increases SZ risk
• What are the concordance rates for MZ twins regarding SZ?

  48%
• What is the concordance rate for DZ twins regarding SZ?

  17%
• What is the risk of developing SZ for parents of affected individuals?

  6%
• What is the risk of developing SZ for uncles/aunts of affected individuals?

  2%
• What is the risk of developing SZ in the general population?

  1%
• What did Tienari et al. (2004) find in their adoption studies?

  Adopted children with SZ parents at risk
• How many adopted children were studied by Tienari et al. (2004)?

  184
• What were the concordance rates for children with SZ biological mothers in Tienari et al.'s study?

  11%
• What were the concordance rates for the control group in Tienari et al.'s study?

  2%
• What does the dopamine hypothesis suggest about SZ symptoms?

  Symptoms arise from abnormal dopamine activity
• What did the original dopamine hypothesis propose?

  Hyperdopaminergia in the subcortex causes symptoms
• Which pathway is linked to positive symptoms of SZ?

  Mesolimbic pathway
• What does the revised dopamine hypothesis propose?

  Hypodopaminergia in the cortex causes negative symptoms
• What is the role of the prefrontal cortex in SZ?

  Helps think logically and organize thoughts
• How is the prefrontal cortex activity related to SZ?

  Lower activity linked to delusions and disorganized thoughts
• What does the basal ganglia affect in SZ patients?

  Affects movement and thinking skills
• How is the basal ganglia related to SZ?

  Larger in schizophrenics causing motor dysfunction
• What is the role of the amygdala in SZ?

  Responsible for basic feelings like fear
• How is the amygdala related to SZ?

  It is smaller in SZ patients
• What research supports genetic explanations for SZ?

  • Ripke et al. (2014) identified 108 genetic variations
  • Brown et al. found correlation between paternal age and SZ risk
• What did Ripke et al. (2014) find regarding genetic variations?

  Identified 108 variations causing SZ predisposition
• What correlation did Brown et al. find regarding paternal age?

  Older fathers have increased risk of SZ
• What is the risk of SZ for fathers under 25?

  0.7%
• What is the risk of SZ for fathers over 50?

  2%
• What are the strengths and limitations of genetic explanations for SZ?

  Strengths:

  • Supported by research findings
  • Identifies genetic predispositions

  
  

  Limitations:

  • Di Forti et al. found drug-induced SZ
  • Suggests genetics is not the only factor
• What practical application does the dopamine hypothesis have?

  Helps in treating SZ with antipsychotics
• What did Curren et al. (2004) find regarding dopamine agonists?

  They can trigger SZ symptoms in non-sufferers
• What did Tauscher et al. (2014) find about antipsychotics?

  They reduce dopamine levels to alleviate symptoms
• What evidence highlights the importance of other neurotransmitters in SZ?

  • Moghaddam and Javitt (2000) emphasized glutamate's role
  • Suggests dopamine hypothesis is limited
• What is the correlation-causation problem in SZ research?

  • Neural correlates linked to SZ symptoms
  • Unclear if symptoms cause reduced activity or vice versa
• What neural correlates are linked to negative symptoms of SZ?

  Activity levels in the ventral striatum
• What is the implication of the correlation-causation problem for SZ research?

  Reduces validity of neural correlates theory