5.3.2 - Carlsson et al (2000)

Question 1

6 x AO1:

Answer 1

• The aim was to review studies into the relationship between levels of neurotransmitters, especially dopamine and glutamate, on symptoms of SZ
• They aimed to use what is known about neurotransmitter functioning and psychosis to provide more of an explanation for SZ than simply the dopamine hypothesis.
• A further aim was to use their understanding of psychosis and links to NT functioning to produce new antipsychotic drugs that could be more effective with fewer side effects.
• The study reviewed research from a variety of sources, investigating neurochemical levels in patients diagnosed with SZ as well as studies into drugs known to induce symptoms of psychosis
• Some research cited found a relationship between levels of glutamate and dopamine production
• Reduced levels of glutamate seems to be associated with increased dopamine release

Question 2

AO3 - Carlsson

5S + 3W

Answer 2

• • The secondary data allows a larger amount of information to be brought together quickly eg that there is a relationship between serotonin and glutamate, and provide an overview of the core findings which would take a long time to gather first hand. Therefore the use of meta-analysis means that valid conclusions can be drawn from the existing evidence in which there is a large amount of detailed information on the topic
• • Relying on secondary data from a variety of different studies means that the reliability and validity of the research is questionable. There is no way for the researchers to know how valid or reliable the original study was. Therefor basing further conclusions about therapeutic options for SZ could be problematic if findings ere originally inaccurate.
• • The results of this study suggest that there are newer drug compounds that may work on levels of other neurotransmitters as well as dopamine. Therefore results have application as it will be very beneficial for patients for whom current anti-psychotic drugs are ineffective
• • Many of the results considered by Carlsson came from animal studies which showed ambiguous results when making claims about excess dopamine which undermines the use of animals when discussing SZ and relevant drug treatment for humans. Therefore conclusions drawn may be invalid as animal findings cannot be generalised to humans due to brain structural differences and cognitive ability
• • Most of the evidence used comes from very reliable and scientific methods eg PET scans and animal studies, which take objective measures of the activity in different areas of the brain. Therefore the conclusions drawn on eg glutamate deficiency leading to excess dopamine, are more valid as there is minimal subjectivity in the interpretation of results when using scientific procedures
• • When discussing the dopamine hypothesis, Carlsson et al suggested that scanning used to look at NT functioning in people might not be valid as being scanned is stressful and can affect ‘normal’ functioning. Therefore findings may not be valid as it could be the environment pp’s were in when being scanned that affected their functioning and that’s not what would be reflected in their everyday NT functioning
• • Sendt et al (2012) found drugs focusing on dopamine do not work on people with SZ and that drugs should focus on glutamate deficiency. They also agree that symptoms in those with SZ seem to come from a dysfunction of glutamate. Therefore this supports Carlsson’s claims and increases the reliability of the conclusions that he made on the influence of glutamate levels
• • The study was ethical as there are no ethical concerns when working with secondary data. Therefore using meta-analysis instead of primary data to look at effective anti-psychotic drugs for those with SZ was ethical when other studies in this area can have ethical concerns due to the vulnerability of the disorder of those involved

Question 3

Conclusion: Carlsson

strong study?

Answer 3

In conclusion Carlsson is a strong study that provides credible evidence that low levels of glutamate has a role in the development of psychotic symptoms which has led to the development of newer drug compounds. However Glutamate deficiency seems to need more research as it may actually be an explanation for SZ, increasing responsiveness to dopamine, giving excess dopamine