Biological explanations

Question 1

What is the genetic explanation for SZ

Answer 1

Polygenic- Sz appears to have a number of genes involved, most likely gene would be those coding for neurotransmitters like DA
Aetiologically heterogenous- different studies have identified different candidate genes shows AH ( different combination of factors including genetic variation can lead to the condition)
RESEARCHERS FOUND- genetic makeup of 37,000 patients was compared to 113,000 controls- 108 genetic variations associated with increased risk of Sz
Role of mutation- Sz can take place in the absence of family histroy of disorder. One explanation for this is mutation in parents DNA for example in parental sperm cells. Can be caused by radiation, food poisoning or viral infection.

Question 2

What is the neural explanation

Answer 2

• research has identified some neural correlates which may be cause of Sz. Best known is dopamine.

Research- Allen et al scanned the brains of patients experiencing hallucinations and compared them to a control group. pre recorded speech. Found lower activation levels in the superior temproal gyrus in hallucination group.

Question 3

evidence for genetic explanation

Answer 3

• There is evidence that schizophrenia runs in families, and so appears to have a genetic basis.
  Gottesman (1991) demonstrated a positive correlation between the increasing genetic similarity of
  family members and their increased risk of developing schizophrenia. The concordance rates are as
  follows = Monozygotic twins (48%), dizygotic twins (17%), siblings (9%) and parents (6%). This,
  particularly due to monozygotic twins sharing 100% of their genes, strongly suggests a genetic
  basis and the existence of candidate genes for schizophrenia. However, it is important to note that
  there are no 100% concordance rates, therefore demonstrating that there are environmental
  influences acting on the
  development of SZ e.g. the
  schizophrenogenic mother and
  dysfunctional thought processing

Question 4

Drug therapy

Answer 4

Typical antipsychotics ( traditional ) - work as a dopamine antagonist, combat positive symptoms of Sz

Atypical antipyschotics ( newer) - combat positive symptoms, also claim to combat negative ones

Question 5

example of typical antipsychotic

Answer 5

Chlorpromazine
- can be taken as tablets, syrup or injection
- works by blocking the DA receptors in the synapses of the brain reducing action of DA
- effectively neutralises neurotransmission in key areas of the brain reducing symptoms like hallucinations

Question 6

example of aytpical antipsychotics

Answer 6

Clozapine
- binds to DA receptors in same way as typical does but in addition acts on serotonin and glutamate receptors
- helps improve mood and reduce depression and anxiety in patients

Risperidone
- binds to dopamine and serotonin receptors
- binds more stronlgy much smaller doses,
- fewer side effects

Question 7

Evaluation for genetic explanation

Answer 7

There is evidence supporting the biological and genetic basis for Sz
Gottsman et al family study- found risk for Sz increases as genetic similarity does. Identical twins 48%, siblings 9%, population 1%
Still 52% unaccounted for when share 100% of genes meaning environment must have an effect. limited explanation on how Sz develops

Question 8

Evaluation for dopamine hypothesis

Answer 8

Evidence for dopamine hypothesis mixed
On one hand there’s evidence that antipsychotics which act as dopamine antagonists by binding to complimentary receptors, alleviating symptoms of Sz, suggesting dopamine has key role in development of Sz in line with dopamine hypothesis
Some researchers criticised dopamine hypothesis for emphasising role of DA too much. For example the neurotransmitters serotonin and glutamate also play a key role as supported by the antipsychotic Clozapine acting upon both of these and being more effective than typical antipsychotics in reducing Sz symptoms