Biological Explanations of Schizophrenia Flashcards
What do family studies have to do with the genetic basis of schizophrenia?
- Family studies have confirmed that risk of schizophrenia increases in line with genetic smiliarity to a relative with the condition
- Kendler et al (1985)- immediate family (first degree relatives) are 18X more a risk.
AND - Gottesman (1991)
Provided supporting evidence for the genetic explanation using family studies
1. Both parents= 46% risk
2. One schiz parent= 16% risk
3. Schiz sibling= 8% risk
4. Grandparent schiz= 5% risk
What did Gottesman & Kendler et al find and what does this suggest about family studies in schizoprenia?
This is A03!
- As concordance rates increase with genetic relatedness, shows that there is a genetic component to schizophrenia.
- The fact that the two studies have similar findings suggests reliability of results, makes conclusions on genetics & schizophrenia more valid.
- However, the results could be from other factors. As first degree relatives are more likely to spend time together than second degree relatives- will have more shared experiences & environments which could also lead to shared behaviours, in this case developing schizophrenia.
- For example, social learning theory may explain that a child may identify with their parent who has schizophrenia & may be more likely to imitate. Therefore, environmental factors may have an influence in the development of schizophrenia.
The fact that fewer than 50% of children where both parents have schizophrenia develop the disorder, suggests therefore there may not be a direct genetic link.
How do the family studies into schizophrenia link with the nature/nurture debate?
- Family members tend to share aspects of their environment as well as many of their genes, so the correlation may represent both factors.
- However, family studies still give good support for importance of genes in schizophrenia.
What do twin studies have to do w the genetic basis of schizophrenia?
- Twin studies compare cocordance rates of schiz between (MZ) & (DZ) twins to show influence of genetics in developing schiz.
- This is because 100% of DNA is shared between MZ twins and 50% In DZ twins.
- In twin study a concordance rate of 74% in MZ twins was found, compared to 24% in DZ, showing a genetic component to schizophrenia.
- Providing evidence for nature nurture debate. - Since MZ concordance rates lay high at 74% it provides strong evidence that schizophrenia is an inherited trait.
- Implying that schiz is a result of nature & argues against idea of a Tabula Rasa, the idea that we are born with minds that are equivalent to ‘blank slates’.
However, there is still 26% of MZ twins that don’t show concordance, therefore it reduces the validity of the biological explanation because if schizophrenia was an entirely genetic trait there would be 100% concordance rates, therefore there may be other environmental factors that are involved with the development of schizophrenia.
One the other hand, the biological explanation of schizophrenia and twin studies as a whole does suffer from biological reductionism, due to the lack of acknowledgement of environmental factors. It is therefore difficult to establish the weighting of whether genetic explanations of schizophrenia is more or less than environmental factors as there are still some environmental factors involved in the development of schizophrenia, due to MZ twins sharing a lot of the same environments.
How do candidate genes have a genetic basis for schizophrenia?
- Early research suggested it was one specific gene that cld explain schizophrenia- but it appears that a number of different genes are invovled:
Steven-Ripke et al (2014): - Looked at genetic makeup of 37,000 people w diagnosis of schiz
- Control group was made up of 113000 & 108 seperate genetic variations were associated w the slightly increased risk of schizophrenia
- This suggests that schizophrenia is etiologically heterogenous (polygenic)
What other research is there into candidate genes supporting the idea that schizophrenia is polygenic?
- Kings college London used 80,000 gnetic samples
- They have found 2000 genomic reigons to be associated w schizophrenia
- So this research also suggests that schizophrenia is polygenic
What can the role of mutation have to do with the basis of schizophrenia?
- Schizophrenia can also have a genetic origin in the abscence of a familt history of the disorder
- One explanation for this is mutation in parental DNA which can be caused by radiation, poison & viral infection
- Evidence for mutation comes from postivie correlations between paternal age (associated with increased risk of sperm mutation) & risk schizophrenia
Brown et al found: - Increasing from around -0.7% with fathers under 25 to over 2% in fathers over 50
What are the different neural correlates that have been associated with schizophrenia?
- Differences in Ventricle Size
- Difference in Brain Activity
- The Dopamine hypothesis
How has the differences in ventricle size been associated with schizophrenia?
- 100 PET scan studies have found enlarged ventircles in the brain of people with schizophrenia
- However, these research findings aren’t consistent
- Although many studies have found enlarged ventricles in the in brains of people w schiz, this is not the case for all people w schizophrenia
- Additionally also not a clear link between enlarged ventricles & symptoms- causual link is not clear
- Also biologically deterministic- suggests a person w enlarged centricles has no control over whether they develop or continue to live w schizophrenia
How has the difference in brain activity been associated w schizophrenia?
- Meyer-Lindenberg et al (2002)
- Examined brain activity in schizophrenics engaged on a working memory task
- Their prefrontal cortex showed reduced activation, reflecting poor performance
- However, it may be that changes in the brain are a result of anti-psychotic medication & were not the cause of schizophrenia
- Ho et al (2005) conducted a longitudinal MRI study investigating the effects on the brain of anti-psychotic medication
- They found that grey matter volumes of all brain regions except for the cerebellum, decreased over time; white matter volume on average was unchanged
- It may be that the differences in schizophrenic brains are not a cause but a consequence of the disorder
What is the dopamine hypothesis?
- Dopamine is a substance that is known to be active in the limbic system, an area of the brain govening emotion- Instrumental in regulating atention- if this process is distrubed it may lead to problems w attention, perception & thought
- The original dopamine hypothesis stated that an excess of neurotransmitter dopamine was implicated in the symptoms of schizophrenia
- Excessive amounts of dopamine or an oversensitivty of the brain to dopamine is linked to some symptoms of schizophrenia
How does the updated dopamine hypothesis specifically work?
- Schizophrenics are thought to have abnormally high numbers of D2 receptors on recieving neurons in the subcorex e.g. limbic system, reuslting in more dopamine binding & therefore more neurons firing.
- More recently, researchers have found that low/abnormal levels of activity in D1 receptors in the perfrontal cortex are associated w negative symptoms of schiz
What evidence is there to support the Dopamine hypothesis?
- Comes from research into effects of antipsychotic drugs which block dopamine activity in brain- found to alleviate symptoms suggesting that the symptoms of schiz are present due to the activity of dopamine in the brain
- Amphetamines are a dopamine agonist & stimulate nerve cells containing dopamine
- They cause the synapse to flood w the transmitter
- High doses of amphetamines cause schizophrenic symptoms, this supports altered dopaminelevels as an explanation for schizophrenia.
Randrup & Munkvad (1966):
- Gave amphetamines to rats, cats & monkeys- led to stereotypical behaviours such as repetitive biting or licking or head movements
- Suggested that this was caused by increase in dopamine in limbic system
Is similar behaviour to stereotyped in human schizophrenic e.g. repetitive behaviour in response to paranoia
- Useful research because can show cause & effect by using animals in an area of study where wld be unethical to use human participants
Give one strength of the biological explanation of schizophrenia.
- Has strong evidence base
- Family studies such as Gottesman show that risk increases w genetic similarity to a family member w schizophrenia
- Adoption studies such as Pekka Tienari et al (2004) show that biological children of parents w schiz are at a heightened risk even if they grow up in an adoptive family
- Twin study by Rikke Hikler et al (2018) showed a concordance rate of 33% for identical twins & 7% for non-identical twins
Further proves some people are more prone to schizophrenia because of their biological make up
Give one limitation for the genetic explanation of schizophrenia.
- Clear evidence to show that environmental factors also increase risk of developing schizophrenia
- The environmental factors include both biological & psychological influences
- Biological risk factors include birth complications & smoking THC-rich cannabis in teenage years (DI FORTI et al 2015)
- 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 w schizophrenia
- Researchers conducted a study- 67% of people w schizophrenia & related psychotic conditions reported at least one childhood trauma as opposed to 38% of a matched control group with non-psychotic mental health problems
This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
Give one strength of the dopamine hypothesis.
- OS: Support for the idea that dopamine (DA) is involved in schiz
- (Curran et al 2004)has shown that by using amphetamines can induce symptoms of schizophrenia in people without schizophrenia & worsen them in people w schizophrenia. This suggests that dopamine plays an important role in the development of schizophrenia.
- Second antipsychotic drugs reduce DA activity & reduce intensity of symptoms - (Tauscher at al 2014)
- Third, some candidate genes act on production of DA or DA receptors
This strongly suggests dopamine is involved in the symptoms of schizophrenia
Give one limitation of the dopamine hypothesis.
- There is evidence for a central role of glutamate
- Post-Mortem & live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people w schizophrenia
- ASW through genetic research several candidate genes for schiz are believed to be involved in glutamate production or processing.
- This means dopamine isn’t only neurotransmitter contributing to development of schiz
- therefore DH is reductionist is it doesn’t consider how other neurotransmitters can affect the development of schizophrenia.
This means that an equally strong case can be made for a role for other neurotransmitters
