Biological explanation

Question 1

AO1: genetic explanation

Answer 1

genetic vulnerability: a genetic component to sz which predisposes some individuals to the illness, suggests its at least partly due to genes

family studies: large scale family study, found individuals who have sz and determine whether their biological relatives have it as-well as non biological relatives. Concluded that the greater degree of genetic relatedness, the greater the risk of developing schizophrenia.

specific genes: sz is polygenic (influenced by 2 or more genes). The candidate genes are PPP3CC and chromosome 5

Question 2

AO3 genetic explanation: limitation-family studies use retrospective data

However, high ecological validity

Answer 2

P: when it comes to family studies they use retrospective data
E: they use patients that have already been diagnosed, meaning they use retrospective data
E: this is unreliable as their may be issues with memory and records. Prospective studies are more reliable as they make comparisons before and after the condition occurs.
L: should take caution when looking at data from family studies
HOWEVER, family studies are high in ecological validity as they are conducted in patients real life environment. Results can be generalised to real life

Question 3

AO1: neural explanation

Answer 3

Dopamine hypothesis: claims that excsessive amounts of dopamine/oversensitivity of the brain to dopamine is the cause of sz. The messages from neurons that transmit dopamine fire to easily/too often. Sz thought to have abnormally high numbers of D2 receptors, resulting in more dopamine binding and more neurons firing

Studied people who took drugs (which increases their dopamine levels), they experienced hallucinations. Also studied people with parkinsons (increases their levels of dopamine), they also had hallucinations. Shows people with sz have high levels of dopamine

hyperdopaminergia is the OG version of the hypothesis. Focuses on high levels of activity/dopamine in the subcortex of the brain

hypodopaminergia is the more recent version. Focused on abnormal dopamine systems in the brains cortex.

neural correlates: measurements of the structure or function of the brain that occur in conjunction with an experiences (sz). Of the negative symptoms, activity in the ventral striatum has been linked to the development of avolition. Of the positive symptoms, reduced activity in the superior temporal gyrus and anterior cingulate gyeus have been linked to the developments of auditory hallucinations

Question 4

AO3: neural explanation; strength- dopamine hypothesis has practical applications

however, cause and effect can’t be established

Answer 4

P: practical applications for dopamine hypothesis
E: led to development of an effective treatment
E: e.g. clozapine, which is more effective than neuroleptics at relieving sz behaviour
L: suggests psychiatrists can understand the role played by neurotransmitters better and therefore improves the patients quality of life
HOWEVER, cause and effect can’t be established from dopamine hypothesis. Are the raised dopamine levels the cause of the schizophrenia or are the raised dopamine levels the result of schizophrenia

Question 5

AO3: neural explanation: limitation- research

Answer 5

P: limitation of research into neural correlates.
E: Research indicated the enlarged ventricles may only explain certain schizophrenia symptoms. Also some non-schizophrenics have enlarged ventricles and vice versa.
E: goes against the idea that sz is linked to a loss of brain tissue
L: implies that research into the role of enlarged ventricles is inconclusive

Question 6

AO3: both explanations: limitation- biologically reductionist

Answer 6

P: both explanations are biologically reductionist
E/E: other factors should be considered such as the family dysfunction explanation of sz
L: need to be aware that the biological explanation doesn’t take into account all factors