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 schizophreniaincreases 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.
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 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 the effects of antipsychotic drugs which block dopamine activity in the 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 rates, 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
- First amphetamines increase DA & worsen symptoms in people w schiz & induce symptoms in people without (Curran et al 2004)
- 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 several candidate genes for schiz 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
