Biological Explanations Of Schizophrenia Flashcards

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1
Q

Describe the genetic explanation of sz.

A

The explanation believes that sz is inherited through genes passed down through families.

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2
Q

What is the concordance rate?

A

The rate of probability that 2 people with shared genes will develop the same organic disease.

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3
Q

What concordance rates did Gottesman find when looking at the heritability of sz and what does this suggest about the onset of sz?

A

6% for parents, 17% for fraternal twins and 48% for identical twins (MZ). It suggests that there is some concordance between the relationship of genetics to someone with sz. If you are related to someone with sz then this increases the chance of developing sz, so there is some genetic component.

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4
Q

What did Gottesman and Shields find in their twin study?

A

Concordance rate of 42% for MZ twins, and 9% for DZ twins. It suggests that there’s a closer genetic relationship to someone with sz as the concordance is higher in MZ than DZ.

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5
Q

What did Heston find in the adoption study and what does this suggest about the onset of sz?

A

Heston compared 47 children of sz mothers who were adopted before the age of 1 month with a control group of 47 children raised by their non-sz adopted mothers. 10% of the children with sz mothers developed it themselves whereas none of the children from the control did. It shows that there is some genetic influence however it does not have a high concordance rate so there is some other influence.

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6
Q

Evaluate a strength of the genetic explanation of sz (supporting evidence).

A

There’s research on families that supports the influence of genes on the onset of sz.
Gottesman found that the closer the genetic relationship, the higher the likelihood of sz development. Only 1% of general population gets sz however if you have a parent with sz it goes up to 6%.
However, it was found that 63% of people with sz did not have any family history of sz.
So this means that the reliability of Gottesman’s research can be questioned even though it suggests there is some genetic influence.

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7
Q

Evaluate a weakness of the genetic explanation of sz (nature vs nurture).

A

It’s difficult to separate biological and environmental factors in research. For example, in family studies, the reason why sz rates are so high (48%) between MZ twins is because they share very similar environments. This means that it is hard to know whether the development of sz is due to genes or the fact they share an environment. This is a weakness as it’s difficult to know the extent to which genes contribute to the onset of sz.

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8
Q

Evaluate a weakness of the genetic explanation (not 100%).

A

Weakness is that the concordance rate for sz is not 100%. In MZ twins, the concordance rate is only 48%. This means there must be another factor which influences the development of sz, like dysfunctional families. This is the idea that people who come from dysfunctional families are more likely to develop sz. This is a weakness as the genetic explanation cannot fully explain the whole onset of sz.

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9
Q

What is the initial dopamine hypothesis?

A

It states that people with sz produces more dopamine than normal brains (hyperdopaminergia). It’s this increased dopamine that is thought to be responsible for some symptoms of sz.

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10
Q

What did Falkai et al find in there post-mortem study?

A

Autopsies have found that people with sz have a larger amount of dopamine receptors. Found an increase of dopamine receptors in brain structures and receptor density. Concluded that dopamine production is abnormal for sz compared to normal controls.

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11
Q

What did Lindstroem et al find in their PET scan study?

A

L-dopa was administered to 10 patients with sz and 10 with no sz diagnosis. PET scans showed the increased utilisation of L-dopa by the sz patients in comparison to the controls. This suggests why szs have excess levels of dopamine.

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12
Q

What is the revised dopamine hypothesis?

A

The role of dopamine in the development of sz has changed over time, with a focus on the limbic system - subcortical areas involved in behaviour like emotion, memory, arousal.

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13
Q

Describe the mesolymbic pathway.

A

The pathway runs from the ventral tegmental area (VTA) to the nucleus accumbens (NA). Too much dopamine in this pathway (neurons firing too often/quickly) causes overstimulation leading to positive symptoms like delusions. Antipsychotic drugs that reduces dopamine transmission (D2 receptors) target this pathway - reducing positive symptoms.

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14
Q

Describe the mesocortical pathway.

A

This pathway runs from the VTA to the frontal lobe. It’s important for emotional response and motivation. Not enough dopamine (hypodopaminergia) in this pathway (D1 receptors) leads to the negative symptoms of sz.

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15
Q

Evaluate a strength of the dopamine hypothesis (supporting evidence).

A

Strength is that there is evidence to support it. For example, Lindstroem et al gave L-dopa to 10 ps with sz and 10 without sz. PET scans increased the utilisation of L-dopa by sz patients compared to controls. This suggests why people with sz have excess dopamine. However the study used a small sample - difficult to generalise. Therefore, even though there is a slight problem with the sample of supporting evidence, there is still good quality to back up the hypothesis.

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16
Q

Evaluate a weakness of the dopamine hypothesis (reductionist).

A

It’s said to be reductionist. It reduces complex sz symptoms down to the action of dopamine in the brain. This means to too simple to say the sz is fully caused by dopamine alone. However, reductionism does allow for scientific study of behaviour as we can look at one explanation closely. Therefore, even though it can be argued that that the dopamine hypothesis as an explanation of sz is too simplistic, it can allow us to understand a potential cause of sz from a scientific viewpoint.

17
Q

Evaluate a strength of the dopamine hypothesis (drug development).

A

Strength is that it has influenced the development of drug therapy. For example, 1st generation antipsychotics were developed as dopamine antagonists - targets the over-production of dopamine. These are effective against positive symptoms. 2nd generation tackled negative symptoms. This means that drugs were developed based on the dopamine hypothesis. Improves the QoL for people by reducing symptoms.

18
Q

Apply the dopamine explanation to antipsychotics.

A

If we know that high/low levels of dopamine in different areas of the brain could be responsible for sz symptoms, then drugs can be developed for this. Antipsychotics are drugs developed to treat disorders by targeting the release of NTs at the synapse. Typical ATs were developed based on the dopamine hypothesis, works by blocking dopamine transmission. Reduces positive symptoms.