Excessive activity (hyperdopaminergic) of dopamine causes schizophrenia because neurons fire too often and transmit too many messages which causes a message overload. As a result, the overload produces schizophrenic symptoms
Juckel 2006 et al. - reduced activity in the ventral striatum is a neural correlate of avolition –involved in motivation which is reduced in avolition therefore abnormality of VS is expected in schizophrenics, negative correlation between levels in VS and severity of overall -ve symptoms
Allen 2007 et al. - reduced activity in superior temporal gyrus and anterior cingulate gyrus are neural correlates of auditory hallucinations – areas less active when hallucination group had to identify pre-recorded speech as theirs or others, made more errors than control group
Gottesman 1991 et al. found greater genetic similarity of the concordance rate for schizophrenia = 48% for MZ, 13% for one parent, 9% for siblings, 6% for parents
Ripke 2014 et al. found 108 separate genetic variations associated with increased risk of schizophrenia; a polygenic condition, differing candidate genes suggests different combos of factors can lead to condition
Tienari 2004 = 6.7% of adoptees with schizophrenic biologicalmother were diagnosed with schizophrenia – reinforces notion that genes create genetic vulnerability to schizophrenia
Birth complications and smoking TCH-cannabis – upbringing makes schizophrenics more vulnerable to developing the condition because it affects psychological and biological state therefore interactionist
Patel 2010 = neural imaging and PET scans found low dopamine levels in dorsolateral prefrontal cortex - PFC is responsible for decision-making and thinking therefore it can account for avolition because it decreases motivation