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  1. Genetic factors are important
    • recurrence rates are high
    • Family risk: 5% of siblings are affected
    • Twin studies: heritability of 60-90%
  2. BARTLETT et al 2012
    have yet to fully understand genetics behind ASD
  3. ARKING et al 2008
    CNTNAP2 observed in those diagnosed with ASD and their relatives
  4. Relatives
    20-30% of relatives are likely to have social and cognitive abnormalities but do not meet criteria of ASD (e.g. may have intense interests but not ASD)
  5. NAVA 2013
    copy number variations on chromosomes 15, 16 and 17 implicated in ASD
    • proposed a variety of factors involved in ASD such as infection and immune dysfunction, metals and neuropeptides. However other studies have yet to find links.
    • Also implicated is the MMR vaccine which has since been shown to be unsupported by evidence
  7. Neurobiology of ASD
    • Enlarged head circumference: normal at birth but gets 10% larger at 3/4 years could be due to poor synaptic pruning
    • Increased cell size and cell packaging density
    • Poor neural connectivity associated with white matter anomalies
    • Very few cross disorder comparisons so cannot conclude if these are ASD specific
  8. AMARAL et al 2008
    • IFG (social impairment and communication)
    • Superior temporal sulcus (communication)
    • Orbitofrontal cortex (repetitive behaviours)
  9. ASD behaviour
    • significant and persistent deficits in social communication and interactions
    • restricted, repetitive patterns of behaviour, interests and activities
    • Symptoms must be present in early childhood
    • Life-long disorder
    • IQ strong predictor of outcome
  10. KANNER 1947
    reported repetitive behaviours, insistence to stick to routine, don’t under jokes (take them literally)
  11. BAIRD et al 2006
    1% of UK population
Card Set:
2013-05-24 13:58:26

Lecture 6
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