Biological Explantation Of Schizophrenia

Question 1

How do family studies support the idea that Sz has a genetic basis?

Answer 1

• Gottesman did a large scale family study. Someone with an aunt with Sz has a 2% chance of developing it, 9% with a sibling and 48% with an identical twin
• Family members also share aspects of the environment

Question 2

How do candidate genes support the idea that SZ has a genetic basis?

Answer 2

• Early research looked for a single genetic variation believing one gene could cause Sz
• however is polygenic - the most likely genes would be coding for neurotransmitters e.g dopamine
• Ripke combined previous data from genome wide studies (look at the whole human genome) in Sz. Genetic makeup of 37,000 people with Sz compared with 113,000 control - 108 genetic variations associated with increased risk
• Sz is aetiologically heterogeneous (different combinations of factors can lead to developing the condition)

Question 3

How does the role of mutation suggest that Sz has a genetic basis?

Answer 3

• Can also have genetic origin in the absence of family history e.g mutation in parental DNA can be caused by radiation, poison or viral infection
• evidence comes from Brown suggesting a positive correlation between paternal age (associated with increased risk of sperm mutation), increasing from around 0.7% in fathers under 25 and over 2% in father over 50

Question 4

How does dopamine relate to Sz?

Answer 4

• research has identified neural correlates (Brian structure/function) associated with Sz, best known is dopamine

Question 5

What is the Original Dopamine Hypothesis?

Answer 5

• based on discovery drugs used to treat Sz (antipsychotics - reduce DA) caused symptoms similar to those with Parkinson’s disease (associated with low DA)
• Therefore Sz may be associated with high DA (hyperdopaminergia ‘hyper’ ‘high’) in subcortical levels of the brain
• excess of DA receptors in pathways from the subcortex to Broca’s area (responsible for speech production) may explain speech poverty/hallucinations.,

Question 6

What is the updated version of the dopamine hypothesis?

Answer 6

• Davis et al proposed the addition of cortical hypodopaminergia (low DA in cortex)
• low DA in prefrontal cortex (thinking) could explain cognitive issues (negative symptoms)
• been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia - both high and low levels of DA in different brain regions
• explaining links between abnormal DA levels and symptoms, also explain origins of abnormal DA function. Both genetic variations and early experiences of stress make someone more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia

Question 7

What research supports the genetic explanation for Sz?

Answer 7

• Tienari adoption studies show that bio children of parents w Sz are at a heightened risk even if they are adopted

Question 8

How is the genetic explanation biologically reductionist?

Answer 8

• environmental factors e.g birth complications and smoking THC-rich cannabis in teenage years
• Also childhood trauma Morkved et al 67% of people with Sz and related psychotic disorders reported childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues

Question 9

What evidence supports neural correlates as an explanation of Sz?

Answer 9

• Curran discovered amphetamines increase DA and therefore worsen symptoms in those with Sz and induces symptoms in those without

Question 10

How does glutamate reduce the validity of dopamine as an explanation for Sz?

Answer 10

• glutamate has a central role, post-mortem and live scanning found raised levels of glutamate in several brain regions (McCutcheon), there may be other neurotransmitters