Biological Explanation of Schizophrenia

• Family Studies


  - family studies have shown that the risk of schizophrenia increases in line with genetic similarity to a relative with the disorder

  
  

  - (Gottesman, 1991) the chance of developing schizophrenia is:

  . 2% if an aunt had it

  . 9% if a sibling had it

  . 48% if the individual was an identical twin

  
  

  - family members tend to share aspects of the environment as well as many of their genes so the correlation represents both; but family studies still support the importance of genes in schizophrenia
• Candidate Genes


  - schizophrenia is polygenic (influenced by multiple genes) the most likely genes would be those coding for neurotransmitters

  
  

  - (Ripke et al, 2014) combined all the data from previous genome-wide studies of schizophrenia:

  . the genetic makeup of 37,00 people with a schizophrenia diagnosis was compared with 113,000 controls

  
  

  . 108 separate genetic variations were associated with slightly increased risk of developing schizophrenia

  
  

  - as different studies had identified different candidate genes it also appears that schizophrenia is aetologically heterogeneous
• Role of Mutation


  - schizophrenia can also have a genetic origin in the absence of a family history of the disorder

  
  

  - one explanation for this is mutation in parental DNA due to radiation, poison or viral infection

  
  

  - evidence for mutation comes from positive correlations between paternal age and risk of schizophrenia increasing from 0.7% in fathers under 25 to 2% in fathers over 50
• Neural Correlates


  - research has identified some neural correlates (a brain structure or function)

  
  

  - the best known neural correlate is dopamine (DA), it is important in the functioning of several brain systems related to the symptoms of schizophrenia

  
  

  - both positive and negative symptoms have neural correlates
• Neural Correlates of Negative Symptoms

  - 1 negative symptoms of schizophrenia is avolition (loss of motivation)

  
  

  - motivation involves anticipation of reward, certain regions of the brain (such as the ventral striatum) are involved in this anticipation

  
  

  - abnormality in these areas may result in avolition

  
  

  - (Juckel et al, 2006) found lower activity levels in the ventral striatum of schizophrenics compared to controls

  
  

  - they also found a negative correlation between activity levels in the ventral striatum and severity of negative symptoms
• Neural Correlates of Positive Symptoms

  - (Allen at al, 2007) scanned the brains of people experiencing auditory hallucinations and compared them to controls whilst they identified pre-recorded speech as their own or others

  
  

  - lower activity levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group who also made more mistakes than the control group

  
  

  - reduced activity in both the superior temporal gyrus and the anterior cingulate gyrus are neural correlates of auditory hallucination
• Original Dopamine Hypothesis


  - the original hypothesis was based on the discovery that drugs used to treat schizophrenia caused symptoms similar to Parkinson's Disease (low DA levels)

  
  

  - high amounts of dopamine activity cause neurons that react to dopamine to fire too often and transmit to many signals leading to a message 'overload'

  
  

  - schizophrenia may therefore be caused by hyperdopaminergia in subcortical areas of the brain (high levels of DA)

  
  

  e.g. excessive amounts of DA receptors in pathways from the subcortex to Broca's area (responsible for speech production) may explain symptoms such as speech poverty and or auditory hallucinations
• Updated Neural Dopamine Hypothesis

  - (Davis et al, 1991) proposed the addition of cortical hypodopaminergia (abnormally low levels of DA) in the brain's cortex

  
  

  - this particularly effects the pre-frontal cortex which is responsible for thinking and decision making

  
  

  - this can also explain negative symptoms of schizophrenia e.g. low DA levels in the prefrontal cortex (responsible for thinking) could explain cognitive problems
• Research Support: Strength

  - the genetic explanation has a strong evidence base

  
  

  - family studies show risk increase with genetic similarity of a relative

  
  

  - (Tienari et al, 2004) show that biological children of parents with schizophrenia are at a heightened risk even if they grow up in an adoptive family

  
  

  - (Hilker et al, 2018) showed a concordance rate of 33% for identical twins and 7 for non-identical twins
• Environmental Factors: Limitation


  - there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia

  
  

  - these included both biological and psychological influences such as:

  . birth complications (Morgan et al, 2017)

  
  

  . smoking THC-rich cannabis in teenage years (Di Forti et al, 2015)

  
  

  - psychological risk factors include childhood trauma :

  . (Morkved et al, 2017) found 67% of people with schizophrenia and related disorders reported at least one childhood trauma compared to 38% of those with non-psychotic mental health issues
• Genetic Counselling: Evaluation Extra

  - our understanding of the role genes play in schizophrenia can be applied to genetic counselling

  
  

  - if one or more potential parents have a relative with schizophrenia they risk having a child that will develop the condition

  
  

  - however the risk estimated by genetic counselling is just an average figure and won't reflect the chance of a child developing schizophrenia as environmental factors play a role
• Evidence for Dopamine: Strength

  - there is support for the idea that dopamine is involved in schizophrenia:

  
  

  . (Curran et al, 2004) amphetamines increase DA and worsen symptoms of schizophrenia and can induce symptoms in those without

  
  

  . (Tauscher et al, 2014) anti-psychotic drugs reduce DA and also the intensity of symptoms

  
  

  . some candidate genes act on the production of dopamine or dopamine receptors

  
  

  - this strongly suggests that dopamine is involved in symptoms of schizophrenia
• Glutamate: Limitation


  - other neurotransmitters may contribute to symptoms of schizophrenia

  
  

  - (McCutcheon et al, 2020) post-mortem and live scanning studies have consistently found elevated levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia

  
  

  - several candidate genes for schizophrenia are believed to be involved in glutamate production or processing
• Amphetamine Psychosis: Evaluation Extra

  - (Tenn et al, 2003) induced schizophrenia like symptoms in rats using amphetamines and they relieved symptoms using drugs that reduced DA action

  
  

  - (Dépatie & Lal, 2001) other drugs that also increase DA level (e.g. apomorphine) don't cause schizophrenia like symptoms

  
  

  - (Garson, 2017) challenged the idea that amphetamine psychosis closely mimics schizophrenia