Biological explanations for sz (AO3 (Not fully comprehensive (Tienari -…
Biological explanations for sz
Gottesman - as genetic similarity increases, so does the probability of sharing schizophrenia.
Candidate genes -
- many genes can increase risk of sz.
- multiple genes can work in combination to produce sz.
Ripke - 108 separate genetic variations associated with inc. risk of sz. These genes were coding for the
functioning of many neurotransmitters
High levels of
dopamine in the subcortex
(central areas of brain). Neurons transmitting dopamine fire too easily/often - positive symptoms.
Abnormally high numbers of
on receiving neurons - more dopamine binding + more neurons firing.
eg. Broca's area - too many receptors = poverty of speech / auditory hallucinations
Abnormal dopamine systems in
Goldman-Rakic - found role for low levels of dopamine in prefrontal cortex (
thinking + decision making
) in -ve symptoms
involved in anticipation of a reward. Abnormality in avolition? No anticipation = no motivation
Juckel et al - found -ve correlation between activity levels in ventral striatum and severity of symptoms. Lower levels of VS in sz than neurotypical
Positive symptoms: reduced activity in
superior temporal gyrus
anterior cingulate gyrus
is a neural correlate of auditory hallucinations.
Not fully comprehensive
Tienari - adoptees who had schizophrenic mothers - 6.7% were also diagnosed, compared to 2% of control. Environment also influences sz - not 100% genetic
Not only neurotransmitter
Moghaddam & Javitt - link between glutamate and sz symptoms, drugs acting on glutamate are more effective than antipsychotics acting on dopamine. Should regulate glutamate not dopamine
Does not always work
Noll - antipsychotics do not work in 1/3 of people - not biological cause for everyone. Should look at different treatments - causes could be: hyp
dopaminergia, dif. NT eg glutamate, psychological cause?
Cannot establish causation with neural correlates
3rd factor! eg. drugs, childhood, upbringing. Could be many explanations for correlation between levels of activity in VS and -ve symptoms. Could be faulty VS causing symptoms? (-ve symptoms may mean less info passes through VS, thus reduced activity)