SCHIZOPHRENIA - Biological explanation for the causes of schizophrenia (sch)

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  • Biological explanation for the causes of schizophrenia (sch)
    • Genetics
      • def: transmission of abnormality by hereditary means
      • sch is passed on genetically - hereditary condition
      • certain genes / variations / mutations of genes
        • no one particular gene causes sch: combination of genes
      • Types of studies
        • gene-mapping
          • def: study into genetic material among sufferers - more knowledge about human genomes
          • DNA of 40,000 schs, and 113,000 non-schs. Identified 128 genetic variations and 108 locations on the human chromosomes the contribute mostly to developing sch
          • Gurling (2006) - gene mapping family study. Identified PCM1 gene which made people more vulnerable to sch
          • difficult to criticise - scientific methods
        • family studies
          • look at young children/adults with sch - look at their relatives and see what level of sch they had
          • the more closely genetically related they are, the higher the con.rate will be (parents over grandparents, for example)
          • high con.rate: more likely you have child with sch with parents who have sch. High con.rates in family members
          • Gottesman (1991) - children with 2 sch parents had con.rate of 46%, children with 1 sch parents - con.rate of 13%, siblings - 9%
          • family members have same environment - growing up with 2 sch parents will make you more sch (NATURE NOT NURTURE)
        • twin studies
          • MZ should be higher con.rate bc they are genetically identical 0 ideally 100%
          • MZ - identical, DZ - non-identical
          • Joseph (2004) - meta-analysis of sch twin studies after 2001: con.rate for MZ twins = 40.4% and 7.4% for DZ
          • very rare to have 100% con.rate for MZ twins (Joseph found 40.4%)
          • some studies use blind diagnosis - researchers don't know if they are testing MZ or DZ twins - those studies have found lower con.rate
          • MZ twins will be treated in the same way (environment) - higher con.rate bc of this, not bc of the genetic similarity
        • Adoption studies
          • use people who are genetically similar but have been raised separately - adopted by diff families
          • high con.rate = shows that it is the genetics not the environment that caused sch
            • arguably better than twin and family studies
          • Tienari (2000) - Finland, 164 adoptees whose biological mums had be diagnosed with sch, 11 (6.7%) had been diag with sch, compared to 4 (2%) of the 197 control adoptees (born to non-sch mums)
          • very small sample sizes - difficult to make generalisations
          • adopted children could be placed selectively - Denmark/US - parents are informed about the genetic background. If they know it - raise in an environment where they are though of as sch -> more likely to develop it
        • Gene mapping
          • DNA of 40,000 schs, and 113,000 non-schs. Identified 128 genetic variations and 108 locations on the human chromosomes the contribute mostly to developing sch
          • Gurling (2006) - gene mapping family study. Identified PCM1 gene which made people more vulnerable to sch
          • difficult to criticise - scientific methods
    • Dopamine Hypothesis
      • def: the development of sch is related to abnormal levels of the hormone and neurotransmitter dopamine
      • schs have more D2 receptors on receiving neurons
        • dopamine increases the rate of communication between neurotransmitters across the synaptic gap
          • too many messages in brain (hearing voices)
      • Evidence to come up with theory
        • Anti psychotic drugs
          • dopamine antagonist - effective
          • reduce dopamine activity in the brain
        • Drug: L-Dopa
          • side effects
          • used to treat Huntingtons disease
          • dopamine agonist (increases impact of dopamine in brain - creates sch)
        • Amphetamines
          • dopamine agonist
          • recreational drugs (eg.speed)
        • Davis (1991) - updated Snyder's theory - high levels of dopamine are not found in sch, and drug clozapine (dopamine-blocking drug) works well
          • high levels in the mesocortical dopamine- negative symptoms
          • high levels of dopamine in mesolimbic dopamine system - positive symps
          • reduced function of the NMDA glutamate receptor in sch. Dopamine receptors reduce release of gluatmate
      • Snyder (1976) - most connected to the positive symps, eg hallucinations, delusions etc
      • Research
        • Patel (2010) - PET scans to assess dopamine levels in sch. Lower levels of dopamine in dorsolateral prefrontal cortex of sch
        • Wang & Deutch (2008) - induced dopamine depletion in the prefrontal cortex in rats -> cognitive impairment (memory deficit) that researchers able to reverse using olanzapine (atypical antipsychotic drug)
      • Evaluation (A03)
        • Leucht (2013) - meta-analysis of 212 studies that analysed the effectiveness of anti psychotic drugs compared with placebo. All tested drugs were significantly more effective than placebo in treatment of pos and neg symps
        • evidence in post-mortem brain tissue has either been negative or inconclusive
        • Moncrieff (2009) - evidence is not conclusive. some drugs have been shown to induce sch episodes but are known to effect other neurotransmitters.
          • points out that other sources of dopamine release have not been considered - stress / smoking etc
    • NOT ON SYLLABUS - Neural correlates (neuro-anatomical)
      • problems with the brain structure
      • enlarged ventricles (gaps in the brain filled with fluid) - common among sch sufferers
      • some schs have large ventricles, some don't - no consistent evidence

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