biological explanation

• Why is misleading neural correlates a problem when we're tying to explain why people develop schizophrenia?


  Neural correlates indicate very little since a cause and effect cannot be inferred, therefore this provides very weak evidence for the biological explanation of schizophrenia.
• What are the three kinds of studies used to investigate the genetic link to schizophrenia?

  Family studies, twin studies, and adoption studies.
• What did Gottesman (1991) find regarding the genetic link to schizophrenia?


  As genes shared with a relative who has schizophrenia increases, so does the person's risk of developing schizophrenia.
• What is the difference between monozygotic and dizygotic twins?

  Monozygotic twins share 100% of their DNA, while dizygotic twins share 50% of their DNA.
• What is the concordance rate of schizophrenia in monozygotic twins?

  40.4%
• What is the concordance rate of schizophrenia in dizygotic twins?

  7.4%
• What is the risk of developing schizophrenia in adoptees with biological mothers diagnosed with schizophrenia?

  7%
• What is the risk of developing schizophrenia in control adoptees?

  1.5%
• What did Ripke et al. (2014) find regarding the genetic variations associated with schizophrenia?

  They found 108 separate genetic variations associated with schizophrenia.
• What are candidate genes?

  Individual genes believed to be a cause of the disorder.
• Is schizophrenia likely to be polygenic?

  Yes, because there is a high number of candidate genes associated with schizophrenia.
• What is the first strength of genetic explanations?

  The supporting evidence for the genetic explanation is particularly strong.
• Why is the evidence for the genetic explanation particularly compelling?

  The evidence for the biological approach comes from a variety of sources such as twin studies, family studies etc. These pieces of research are scientific as they are objective and based on empirical data.
• Why is strong evidence a strength for the biological explanation of schizophrenia?

  If the supporting evidence is strong, this increases our confidence in the validity of the biological explanation of schizophrenia.
• What is a limitation of the genetic explanation of schizophrenia?

  There is clear evidence to show that environmental factors also increase the risk of developing schizophrenia
• What environmental factors also increase the risk of developing schizophrenia?

  Biological risk factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma
• Why are environmental risk factors a weakness of the genetic explanation of schizophrenia?

  This reduces the validity of the biological explanation of schizophrenia as it points towards other factors that are involved and this theory cannot be used alone to explain the development of the disorder
• Is there hypodopaminergia or hyperdopaminergia in Broca's area?


  Hyperdopaminergia
• What is a second limitation of the genetic explanation of schizophrenia?


  There are also consequences to assuming a genetic basis to schizophrenia
• What are the consequences to assuming a genetic basis to schizophrenia?

  Place responsibility on the family, this could lead parents to feeling blamed for passing on genes that caused the disorder. It also suggests a level of determinism
• What do the consequences suggest about the genetic explanation of schizophrenia?

  Suggests that the genetic explanation of schizophrenia is a sensitive one, leading to the need to provide genetic counselling and have caution in how we explain this to those affected by the disorder
• What are neural correlates?

  Measurements of brain structure/function that correlate with an experience.
• What neurotransmitter is believed to be involved in schizophrenia?

  Dopamine.
• What is the dopamine hypothesis?

  The hypothesis that dopamine abnormalities contribute to schizophrenia.
• What did the original dopamine hypothesis focus on?

  High levels or activity of dopamine in the subcortex.
• What are high levels of dopamine called?

  Hyperdopaminergia
• What were high levels of dopamine thought to be caused by?

  An excess of D2 receptors
• What is the revised dopamine hypothesis?

  Both excess and deficit of dopamine can contribute to schizophrenia.
• What is a deficit of dopamine called?

  Hypodopaminergia
• how is excess dopamine affecting Broca's area?

  May be associated with poverty of speech and auditory hallucinations.
• What did Allen et al. (2007) do?

  Scanned the brains of people experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs or others
• What did Allen et al. (2007) find?

  Low levels of activity in the superior temporal gyrus when participants with schizophrenia listened to their own and other's voices
• What does the superior temporal gyrus contain?

  The auditory cortex
• What could low activity in the superior temporal gyrus be causing?

  Auditory hallucinations
• What did Juckel et al (2006) find?

  Low levels of activity in the ventral striatum
• What is the ventral striatum responsible for?

  Anticipating rewards
• What could low activity in the ventral striatum be causing?

  Avolition
• What is the first strength of the dopamine hypothesis?

  Supporting evidence
• What is the supporting evidence for the dopamine hypothesis?

  Amphetamines increase dopamine and worsen symptoms in people with schizophrenia and induce symptoms in people without (Curran et al. 2004). Second, antipsychotic drugs reduce dopamine activity and reduce the intensity of symptoms (Tauscher et al. 2014). Third, some candidate genes act on the production of dopamine or dopamine receptors.
• What is a second strength of the dopamine hypothesis?


  Real life applications