Biological Explanations

• Biological Explanation: Genetic Factors

  Schizophrenia tends to run in famileis but only genetically

  No one gene is thoguht to be more responsible for this disorder - its more likely a combination however having these genes does not mean you WILL develop schizophrenia
• Family studies

  GOTTESMANN (1991) confirmed that the risk of schizophrenia increases in line with genetic similarity to a relative with the condition so the closer the degree of genetic relatedness, the higher the risk
• Twin studies:

  If monozygotic twins are more concordant than dizygotic then this suggests greater similarity is due to genetic factors

  JOSEPH (2004) calculated that the pooled data for all schizophrenia twin studies showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins
• Adoption studies:

  Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are used

  TIENARI et al (2000) found:

  Of the 164 adoptees whos biological mothers has schizophrenia, 11 recieved a diagnosis aswell. Investigators concludeed that these findings showed that the genetic liability to schizophrenia had been 'decisively confirmed'
• Candidate genes are individual genes that are associated with a risk of inheritance - Schizophrenia is believed to be polygenetic with the most likely gene is dopamine

  RIPKE et al (2014) carries out a study combining all previous data from genome-wide studies

  He found 108 seperate genetic variations were associated with the risk including those that code for neurotransmitters
• There can be a genetic origin in the absence of a family history of the disorder. One explanation of mutation in parental DNA - can be caused by radiation or viral infection or poison

  BROWN et al (2002) positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia. Also increasing from 0.7% with fathers under 25 to over 2% in fathers over 50
• Hyperdopamergia:

  OG version of the hypothesis; focuses on the possible role of high levels or activity of dopamine in the subcortex. OVERACTIVE
• Hypodopmanergia:

  Recent version of the hypothesis; focuses on low level dopamine and the abdominal dopamine systems in the brains cortext - particularly the pre-frontal cortex which is responsible for thinking and decision making

  
  

  GOLDMAN-RAKIC et al(2004) identified a role for low levels of dopamine in the prefrontal cortex in the negative symptoms
• Evaluation of Dopamine hypothesis

  STRENGTH: support for the idea dopamine is involved

  1. Amphetamines increase dopamine and worsen symptoms in people with schiz and induce symptoms in people without (CURRAN et al 2004)
  2. Antipsychotic drugs reduce dopamine activity and also reduce the intensity of symptoms (TAUSCHER et al 2004)
• Evaluation of Dopamine hypothesis

  Limitation: Glutamate

  1. Post-mortem and live scanning studies have found levels of the neurotransmitter glutamate in several brain regions of people with schiz
  2. Several candidate genes for schiz are believed to be involved in glutamate production or processing
• Biological Explanation: Neural correlates

  One negative symptom avolition involves the loss of motivation which involves anticipation of a reward certain regions of the brain are believed to be particularly involved in the ventral striatum

  JUCKEL et al (2006) measured activity levels in the ventral striatum and found lower levels of activity than those observed and there was a negative correlation between activity levels in the VS

  Therefore the VS is a neural correlate of negative symptoms