Biological Explanation Flashcards
Outline genetic basis of SZ
-notes for many years that SZ runs in families
-strong relationship between degree of genetic similarity and shared risk of SZ, Gottesman found 48% for MZ and 17% for DZ
Limitation of genetic basis explanation
Family members tend to share aspects of their environ as well as genes
What are candidate genes
Individual genes that are believed to be associated with risk of inheritance, SZ appears to be polygenic
How is SZ aetiologically heterogenous
Different combinations of factors can lead to the condition
What did Ripke find in study about genetic basis of SZ
Compared genome of people diagnosed with SZ with controls, 108 genetic variations associated with increased risk of SZ including those coding for the functioning of a number of NTs including dopamine
Explain dopamine hypothesis
-Hyperdopaminergia in subcortex- og version, focused on possible role of high levels/activity of dopamine in subcortex and dopamine pathway from subcortex to Broca’s area May be associated with speech poverty and auditory hallucinations
-Hypodopaminergia in cortex- more recent version, research identified role for low levels of dopamine in PFC (thinking and decision making) in negative symptoms (may be specifically avolition)
What are neural correlates
Measurements of the structure/function of the brain that correlate with SZ
Neural correlates of negative symptoms and who found this
Avolition: abnormality of areas eg ventral striatum that are involved in the anticipation of reward, Juckel found lower levels of activity in ventral striatum in those with SZ compared with those without. Also observed negative correlation between activity levels in VS and severity of overall negative symptoms
Expand on strength that multiple sources of evidence for genetic susceptibility
-eg Gottesman shows how genetic similarity and shared risk of SZ are closely related and adoption studies show children of people with SZ are still at heightened risk even if adopted into families with no history of SZ, suggests genetic factor important
Expand on limitation that cannot conclude causation
-possible that negative symptoms mean less info passes through striatum leading to reduced activity or another factor may influence both the negative symptoms and ventral striatum, may truly tell us very little
Expand on strength that there is evidence for role of dopamine
-eg dopamine agonists that increase levels of dopamine make SZ worse and can produce SZ-like symptoms in people not diagnosed/antipsychotics work by reducing dopamine activity suggesting dopamine has important role
