Biological explanation for SZ Flashcards
(14 cards)
What have family studies confirmed about SZ?
-SZ runs in families
- Gottesman large scale family study how a closer relationship with a person with SZ increases the chances of developing SZ.
E.g. 2% if uncle has it, but 48% if identical twin has it.
What do Genetics show about SZ?
- SZ is Polygenic: Multiple genes are involved in development of SZ
- Those most likely implicated are those coding for neurotransmitters.
E.g. Dopamine
How can the age of your father influence SZ development?
- Evidence for mutation comes from positive correlations between parental age (sperm mutation)and the risk of SZ increasing from 0.7% with fathers under 25 to over 2% in fathers over 50.
What is meant by Neural correlates?
Brain structure and function influencing development of SZ.
Outline the Original Dopamine Hypothesis.
-High levels of dopamine (hyperdopaminergia) in subcortical brain areas is associated with hallucinations and poverty of speech or auditory hallucinations.
- An excess of DA receptors in pathways from the subcortex to broca’s area.
(explaining speech poverty etc)
Outline the updated Dopamine hypothesis.
-Abnormally low levels of DA in the brains prefrontal cortex (responsible for thinking) can explain negative symptoms.
- Suggested cortical hypodopaminergia leads to subcortical hyperdopaminergia.
- It explains the origins of abnormal DA function, such as early experiences of stress make some people more sensitive to hypodopaminergia and therefore hyperdopaminergia.
What is the Glutamate hypothesis in SZ?
- SZ symptoms and cognitive impairment are due to hypofuntion of NMDARs and excessive glutamate release, especially in brain areas including the prefrontal cortex.
What is Parkinson’s disease?
- Parkinson’s is a degenerative condition which all cells in the substantia nigra die.
- Resulting in reduced dopamine level.
- Affects the brains ability to control body movements.
One strength of the genetic explanation is the strong evidence base Family studies such as Gottesman.
Family studies such as Gottesman show that risk increases with genetic similarity to a family member with schizophrenia. Adoption studies such as Tienari, show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family. A recent twin study by Rikke Hilker showed a concordance rate of 33% for identical twins and 7% for non-identical twins.
This shows that some people are more vulnerable to schizophrenia as a result of their genetic make-up.
One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia.
These environmental factors include both biological and psychological influences. Biological risk factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia.
In one study, 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
One strength is support for the idea that dopamine (DA) is involved in schizophrenia.
First, amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without (Curran et al. 2004).
Second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms (Tauscher et al. 2014).
Third, some candidate genes act on the production of DA or DA receptors.
This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
One limitation of the dopamine hypothesis is evidence for a central role of glutamate
Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia (McCutcheon et al. 2020).
In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.
This means that an equally strong case can be made for a role for other neurotransmitters.
