biological explanations for sz Flashcards
family studies AO1 + AO3
risk of sz increases with genetic similarity to a relative with the disorder - research support from irving gottesman 1991 large scale fam study: 48% risk of sz with an identical twin, 9% risk with a sibling
research support: gottesman fam study
risk increases with genetic similarity
Tienari et al - adoption studies
bio kids of parents with sz are at greater risk even if raised in an adoptive fam
Hilker et al - twin studies - concordance rate of 33% for identical twins and 7% for non-identical twins.
what are candidate genes ao1
og belief - 1 single faulty gene could cause sz
many genes involved - sz is polygenic, the genes would typically be those involved in coding for neurotransmitters - eg dopamine
research support: Ripke et al 2014
combined data from genome wide studies of sz
genetic makeup of 37000 szs compared to 113000 controls = 108 separate genetic variations associated with sz risk.
diff studies have diff candidate genes - sz is aetiologically heterogeneous = diff combos of factors can cause sz.
limitation of the genetic explanation ao3
environmental factors also increase risk of sz = includes bio and psych influences
bio - birth complication Morgan et al 2017 + smoking THC rich cannabis in teen yrs Di forti et al 2015
psych = childhood trauma - more vulnerable to adult mh issues but specific to sz - Morkved et al 2017:
67% szs + related psych disorders reported at least 1 childhood trauma | 38% matched grp with non-psych mh issues
genetic factors alone cannot provide a complete explanation for sz
what is neural correlates
a brain structure / function
original dopamine hypothesis ao1
sz is due to high levels of DA - hyperdopaminergia - in subcortical areas of brain
eg. excess of DA receptors in pathway from subcortex to Broca’s area may explain specific symptoms of sz such as speech poverty/ hallucinations
based on Seeman 1987- antipsychotics (lower DA levels) causes symptoms similar to those in ppl with Parkinsons’ - associated with low DA levels.
evaluate the original dope hyp
support: Curran et al 2004
amphetamine increases DA + worsens SZ symptoms + induces symptoms in normals
antipsychotics reduce DA activity + reduce intensity of symptoms - Tauscher et al 2014
some candidate genes act on the production of DA/ DA receptors
limit: McCutcheon et al 2020
evidence for central role of glutamate
post-mortem + love scanning studies consistently found raised levels of nt glutamate in many brain regions of ppl with SZ
several candidate genes for SZ involved on glutamate production/ processing
updated version of the og dope hyp ao1
Kenneth davis et al 1991 - addition of cortical hypodopaminergia = low DA in cortex
low DA in prefrontal cortex = explain cognitive issues
cortical hypo DA could lead to subcortical hypo DA - both high and low levels of DA in diff brain regions
