BIOLOGICAL EXPLANATIONS

• GENETICS 


  Schizophrenia runs in families: comparing individuals with schizophrenia to biological and non-biological relatives.
• FAMILY STUDIES 


  The more closely related  (genetic similarity) the greater the likelihood of developing schizophrenia.   Relatives with schizophrenia = risk factor increases (6-17%).
• TWIN STUDIES 


  • Twin studies - MZ (100% genes) vs DZ (50% genes).  Concordance rates show 40.4% (MZ) vs 7.4% (DZ).
• ADOPTION STUDIES


  Comparing twins who have been adopted with incidence of schizophrenia to biological and adoptive parents.  Biological = genetic, adoptive = environment. 
• CANDIDATE GENES


  Early research looked unsuccessfully for a single genetic variation to explain sz. sz is polygenic - requires several genes. it is also aetiologically heterogenous - risk is affectd by different combinations
• MUTATION 


  SZ can also have a genetic origin in the absence of a family history because of mutation in parental DNA
• NEURAL CORRELATES 


  Sz is related to structural and functional brain abnormalities, measured using advances in brain scanning technology, e.g. fMRI or the role of neurotransmitters.  Brains are compared with non-sufferers, with tasks such as cognition, thought processing and working memory.  
• NEURAL CORRELATES 


  +VE SYMPTOMS

  • Hallucinations develops due to lower activation levels in the superior temporal gyrus (contains the primary auditory cortex, deals with sound) and anterior cingulate gyrus (deals with conflict and error monitoring).
• NEURAL CORRELATES 


  -VE SYMPTOMS

  • Avolition (loss of motivation) = abnormalities (lower levels of activity) in the ventral striatum (associated with the anticipation of rewards).  
  • Enlarged ventricles (brain cavities filled with cerebrospinal fluid) = patients displaying negative symptoms. 
• NEURAL - DOPAMINE 


  It is widely believed to be involved in sz because it is featured in the functioning of the brain systems related to the symptoms of sz
• DOPAMINE - ORIGINAL THEORY

  Hyperdopaminergia in the subcortex - high levels of dopamine in the central areas of the brain (subcortex), e.g. an excess of dopamine receptors from the subcortex to the Broca’s area may be associated with poverty of speech and/or the experience of auditory hallucinations.  This is due to messages firing too often. 
• DOPAMINE - UPDATED THEORY

  Hypodopaminergia in the cortex - low levels of dopamine in the prefrontal cortex (thinking and decision making) associated with negative symptoms.
• (+) GENETICS


  GOTTESMEN =

  reported that the concordance rate for twins raised apart was

  very similar to those brought up together. This suggests that high concordance rates for identical twins was not due to them being treated in a similar way by the family, i.e environmental factors had little effect on the development of schizophrenia. (-) However, the concordance rate is not 100% therefore it cannot be completely caused by genes.
• (-) GENETICS 


  TWIN STUDIES the assumption that the environments of MZ twins and

  DZ twins are similar. = assumed that the higher concordance rates in MZ twins is because of higher genetic similarity. JOSEPH = it is widely accepted that MZ twins are treated more similarly, encounter more similar environments e.g more likely to do the same things, and more likely to experience identity confusion i.e being treated like ‘twins’ rather than individuals. = differences in concordance rates between MZ and DZ twins reflect nothing more than the environmental differences.
• (+) GENETICS


  ADOPTED STUDIES =

  TIENARI found that 10.3% of adopted children who had

  schizophrenic mothers also developed schizophrenia, compared to only 1.1% of children without schizophrenic mothers.
• (-) GENETICS


  these studies also show the environment to be an important factor. Children at genetic risk because of schizophrenic mothers had good psychological health if raised by an adopted families low in communication deviance (i.e they communicated very clearly). This suggests that although genetic factors are important in the development of schizophrenia,

  environmental factors are also important.
• NEURAL - DOPAMINE 


  • Antipsychotic drugs used to treat schizophrenics have the ability to block dopamine receptors and therefore reduce symptoms of schizophrenia.
  • The use of a drug called L-dopa which has the ability to increase dopamine levels has been used on animals and shown to produce many of the symptoms of schizophrenia.
  • And finally, post mortem examinations have shown that patients with schizophrenia have higher densities of dopamine receptors in certain parts of the brain than those without.
• (-) DOPAMINE 


  it is very difficult to measure an individual's dopamine levels, except either by post mortem examination or by taking fluid from the spine.
• (+) DOPAMINE 


  with the development of brain imaging techniques they are starting to provide more detailed evidence. WONG found that individuals with schizophrenia had more than twice as many dopamine receptors than the control group.
• (+) DOPAMINE 


  success of drug treatments that attempt to change dopamine activity in the brain. E.g LEUCHT ET AL carried out a meta-analysis of 212 studies that had analysed the effects of different antipsychotic drugs compared with a placebo. They found that all drugs tested were significantly more effective than the placebo in the treatment of positive and negative symptoms, achieved through the normalisation of dopamine
• (-) DOPAMINE 


  MONSIEF =

  claims that the evidence for the dopamine hypothesis is far from

  conclusive, e.g although stimulants such as cocaine have been shown to induce schizophrenic episodes, such stimulants are known to affect many neurotransmitters other than dopamine. also pointed out that other sources of dopamine release e.g. cigarettes have not been

  considered. Therefore the theory that schizophrenia is caused by overactivity of the dopaminergic system is not fully supported by current evidence.