contemporary study: carlsson (1999) (20)

Question 1

para 1

Answer 1

AO1: aims
->to review studies into the relationship between NT levels, especially dopamine & glutamate, on symptoms of sz
->another aim is to explore a rival theory, that of glutamatergic deficiency or hypoglutamatergia
->to consider the need for further research into drug treatments that target NTs other than dopamine

AO3: strength
->Carlsson’s study had high generalisability as it used findings from 32 different studies with a large sample.
->as they used secondary data from a unde variety of studies, they gathered a huge sample, allowing a precise
estimate of the effect of NTs on symptoms of SZ.
->therefore greatly increasing the ity of his findings to a wider population

AO3: weakness
->Carlsson used previous research that used rodents to test NT and function
->Miller and Abercrombie studied glutamate levels in rats. They found that as dopamine levels increase, glutamate activity decreases by blocking NMDA
->the findings show glutamate as a factor for SZ cannot be generalised to humans as animals have less developed brain regions than humans.

Question 2

para 2

Answer 2

AO1: method
->Carlsson used secondary data by conducting a literature review of 32 other studies
->eg. they studied
Lindstroem et al (1999), who labelled a chemical L - Dopa, & administered it to 10 patients with SZ, & 10 without
->The L-Dopa was taken up quicker in patients with SZ, suggesting that they had more D2 receptors than
the control group

AO3: strength
->high reliability
->much of the research used in the review comes from PET scans
->eg. Lindstroem used PET scans to see that L- Dopa was taker up quicker in SZ patients than a control group.
->standardised procedure
replicable, increases reliability

AO3: weakness
->Carlsson’s study has low reliability as there’s no standardised procedure
->his results came from looking at numerous other studies
->therefore can’t be replicated, which
decreases reliability of findings.

Question 3

para 3

Answer 3

AO1: findings
-> they found 2 types of cause for s2
->hyperdominergia (too much dopamine, which can be treated by FGAs)
->hypoglutamatergia (too little
glutamate, which can be treated by TGAs)

Question 4

para 4

Answer 4

AO1: conclusions
->SZ may have different types, which can be caused by abnormal levels of different NTs, not just dopamine
->further research needs to be conducted in developing drugs to treat SZ that avoid negative side effects