Biological explanations for Schizophrenia

Question 1

A01

Outline the genetic basis of SZ-Family studies

Answer 1

Family studies confirm there is a genetic vulnerability for SZ that increases in line with genetic similarities between family members
Gottesman(1991) found:
If both parents suffer from SZ ,- 46%
one parent-13%
A sibling with SZ , 9%
Compared to 1% chance via genetic connenction to general population
The more genetically similar relatives are(identicial twins) the higher concordance rate for SZ

Question 2

A01

Outline the role of Candidate genes in SZ

Answer 2

SZ is polygenic
Ripke et al (2014) Found that up to 108 different gene variations were associated with higher risk of devloping SZ
Sz is thus aetiologically heterogenous meaning there is more than one genetic origin of SZ & different combinations of genes can lead to SZ

Question 3

A01

Outline the role of muation-Brown

Answer 3

There is a risk of SZ developing even if there no history of it in family, due to genes that mutate

Mutation comes from anything that alters the DNA, e.g - poisoning, radiation or viral infection

Brown et al. (2002) found positive correlations between parental age & risk of developing Sz, increasing from 0.7% in fathers under 25 years of age, to over 2% in fathers over 50 years of age (stemming from an increased risk of sperm mutation)

Question 4

A01

Outline the neural correlates of SZ

Answer 4

The neural correlate of SZ is the neurotransmitter dopamine (DA)
The original hypothesis based on discovery that drugs used to treat SZ ( antipsychotics, reduce DA)
thus SZ may be result of high levels of DA ( hyperdopamininergia) in subcortical areas of the brain
e.g excess of DA receptors in pathways from the subcortex to Brocas area (responsible for speech production) may explain specific symptoms of SZ such as poverty of speech /auditory hallucinations**

Question 5

A01

The original dopamine hypothesis

Neural correlates for SZ

Answer 5

The original dopamine hypothesis suggests that hyperdopaminergia (abnormally high dopamine levels) in the subcortex is responsible for SZ,

whereas most recent versions of dopamine hypothesis suggests
hypodopaminergeria (abnormally low dopamine levels) in the cortex is more likely to be responsible for SZ.
The modern understanding is that both hyper- & hypodopaminergia in
different areas of the brain contribute to the development of SZ.

Question 6

A03

Research support for genetic explantion-Hilker

strength

Answer 6

Research studies by Gottesman show risk increases with genetic similarity to a family member with SZ
Twin studies Hilker et al(2018) show a concordance rate of 33% for identical twins & 7% for non identical twins
shows people are more vulnerable to SZ as a result of genetic makeup

Question 7

A03

Evidence for dopamine as a neural correlate for SZ-amphetamines

Answer 7

One strength is support for the idea that (DA) is involved in SZ
first, amphetamines increase DA & worsen symptoms for people with SZ & induces symptoms in people without ( Curran et al)
2nd, antipsychotic drugs reduce DA activity & also reduce intensity of symptoms ( Tauscher et al)
3rd some candidate genes act on production of DA or DA receptors
strongly suggests that DA is involved in symptoms of SZ

Question 8

A03

strength of neural correlates of SZ-brain imaging techniques

Answer 8

The use of brain imaging techniques such as PET, MRI & FMRI provide objective evidence for neural correlates of schizophrenia as they pinpoint specific brain structures implicated in the symptoms of the disorder
brain imaging technologies are conducted under controlled clinical conditions means likely show consistent results over time -reliable

Question 9

A03

Limitation of neural correlates of SZ

Answer 9

• research evidence for neural correlates takes a correlational approach to mapping brain regions to SZ means it lacks cause & effect explanations
• There is no acknowledgement of the role of enviroment to a neural correlate -based explanation of sz means lacks external valdiity