Biological explanations

• Family studies into schizophrenia

  Gottesman's large-scale family study (1991) confirmed risk of schizophrenia increases in line wth genetic simularity, however family members tend to be exposed to the same enviroment causing a correlation between genetics and enviroment.
• Candiate genes

  Multiple gees are involved in the diagnosis of schizophrenia (it is polygenic)

  Ripke et al (2014) conclded that schizophrenia is aetiologically heterogeneous (combination of factors e.g. genetic variation
• Mutation in schizophrenia

  SZ can be caused by mutated parental DNA (radiation, poison or infection) Evidence comes from positive correlations with paternal age and risk of SZ. 0.7% with fathers under 25, 25 with fathers over 50. (Brown et al, 2002)
• Twin studies in SZ

  Joseph (2004) - MZ twins are treated much more similarly than DZ twins as they are treated more as a pair than individuals.
• Adoption studies

  Tienari et al ( 2000) found that 164 adoptees whos biological mothers had SZ , 6.7% also received a diagnosis compared to 2% of the 197 'control' adoptees (born to non- SZ mothers)
• Environmental factors affecting SZ.

  Clear evidence showing that environmental factors also alter the risk of a diagnosis. Morgan et al (2017) - smoking THC rich cannabis in teenage years, Di Forti et al (2015) Childhood trauma making people more vunerable to developing SZ.

  Morkved et al (2017) found that 67% of psychotic patients reported at least one childhood trauma as opposed to the 38% of a matched group with no mental health issues.
• The role of dopamine

  Dopamine is responsible for feelings of pleasure. It effects thinking and movement.
• What is Hyperdopaminergia?

  High levels of dopamine in the sub cortex, an excess of dopamine receptors in the Broca’s area may be associated with speech poverty and auditory hallucinations.
• What is Hypodopaminergia?

  Low levels of dopamine in the cortex. linked to the negative symptoms of SZ (Goldman-Rakic, 2004)
• David and Kahn (1991) research into dopamine.

  Positive symptoms caused by and excess of dopamine in the subcortical areas of the brain (ie. the mesolimbic pathway)

  Negative symptoms = deficit of dopamine in the prefrontal cortex (mesocortical pathway)
• Research support for the dopamine hypothesis.

  Drug therapy.

  L dopa - parkinsons medication, increases dopamine which may produce symptoms similar to that of SZ
• Limitations of the dopamine hypothesis.

  Drugs were ineffective for 1/3 of patients. Suggesting dopamine cannot explain all cases.
• Strengths of genetic explanations for SZ.

  Strong evidence/research base.

  Gottesman (1991) Increased risk with increased genetic similarity.

  Tienari et al (2004) Children with the same genetics but a different environment are still at risk of developing SZ.
• Neural correlates in SZ

  These are changes in neural events and mechanisms that result in the characteristic symptoms of a behaviour/mental disorder. There is growing evidence that SZ is linked to structural abnormalities
• Neural correlates (ventricular space)

  People with SZ have abnormally large ventricles in the brain, making them lighter than normal.
• Neural correlates (avolition and ventral striatum)

  Activity in the ventral striatum is found to be linked to anticipation of reward. Therefore if this area is abnormal, this may result in avolition.
• Neural correlates (hallucinations and superior temporal gyrus)

  Patients experiencing auditory hallucinations have showed lower activation levels in these areas.
• Neural correlates (affective flattening and amygdala)

  The amygdala is responsible for basic feelings, eg. fear, hunger .In SZ patients the amygdala is smaller, leading to loss of emotion (affective flattening)
• Neural correlates (disorganised thoughts and pre-frontal cortex)

  Many patients have lower activity in their pre-frontal cortex (the pre-frontal cortex helps people think logically and organise their thoughts) This could link to delusions and disorganised thoughts.