Lesson 2 – Biological Explanations of Schizophrenia

Question 1

What the two biological explanations of schizophrenia

Answer 1

Biological explanations of schizophrenia are based on two factors: the genetic basis and neural correlates including the dopamine hypothesis.

Question 2

How is the genetic basis of schizophrenia tested

Answer 2

Genetic factors are normally tested through family, twin and adoption studies

Question 3

Family studies for schizophrenia

Answer 3

Gottesman (1991) found that if both parents were schizophrenic, then the likelihood of the offspring also having SZ was 46%, if one parent was schizophrenic, then the likelihood dropped to 13% and if a sibling (brother or sister) had SZ, the likelihood was 9% - this study shows that the more closer you are genetically related the more likely you are to get SZ.

Question 4

Twin studies for schizophrenia

Answer 4

As Monozygotic twins (MZ) (identical twins) share 100% of their genes whereas as Dizygotic twins (DZ) (non-identical) twins share 50% of their genes, if SZ is genetic, then the concordance rates should be much higher for MZ rather than DZ twins! Gottesman (1991) found a 48% concordance rate for MZ twins and 17% concordance rate for DZ twins- this study shows that the more genetically similar you are then the more likely you are to get SZ.

Question 5

Adoption studies for schizophrenia

Answer 5

Tienari et al (2001) carried out a study in Finland. 164 adoptees whose biological mothers had been diagnosed with SZ, 11 (6.7%) were also diagnosed with SZ compared to a control group of 197 adoptees where only 4 (2%) were diagnosed with SZ. This study shows that although the overall percentage of children (who have been adopted by non- schizophrenic parents) having SZ was very low, as there was a small link between genes and SZ with children whose biological mothers were schizophrenic.

Question 6

Candidate genes for schizophrenia

Answer 6

There are specific candidate genes that seemed to be associated with SZ (such the the PCM1) although it is now agreed that SZ is polygenic – this means that there is a combination of different genes that have been implicated in SZ.

Question 7

Candidate gene evidence from family studies

Answer 7

Gurling et al (2006) used evidence from family studies indicating that SZ was associated with chromosome 8p21-22 to identify a high-risk sample. Using gene mapping, the PCM1 gene was implicated in susceptibility to SZ, providing more evidence for genetics. Also Benzel et al. (2007) used gene mapping to find evidence suggesting that NRG3 gene variants interact with both NRG1 and ERBB4 gene variants to create susceptibility to developing SZ, suggesting an interaction of genetic factors.

Question 8

Candidate gene evidence from genetic makeup

Answer 8

Ripke et al (2014) compared the genetic makeup of 37000 SZ patients worldwide with 113000 controls. They found that 108 separate genetic variations were associated with an increased risk of SZ. The genes that were particularly vulnerable were the ones that had some connection to the functioning of certain neurotransmitters such as dopamine.

Question 9

Strengths of the genetic basis for schizophrenia

Answer 9

There is a wealth of research evidence to support the genetic basis for SZ as can be seen from the findings of Gottesman, Joseph’s and Tienari’s study, thus there is a link between genes and SZ. This is a strength because it shows that if a child grows up in a family where both their biological parents has SZ, then the chances of them getting it is heightened compared to if only one parent or none of the parents have it suggesting that genetics is an important factor.

Question 10

Weaknesses of the genetic basis for schizophrenia

Answer 10

The problem with twin and family studies is separating nature (genes) from nurture (the environment). For example, MZ twins are normally reared together and sent to the same school, where the same clothes (in childhood), this then makes it difficult to separate upbringing from genes. Even if we look at adoption studies that attempt to separate genes from the environment, children tend to be adopted by relatives who may still rear the child similarly to its biological parents – thus adoption studies may not always be a good comparison for the effects of nature and nurture.

The Genetic explanation of SZ is also biologically reductionist as it is stating that one cause of SZ is simply your genes. In other words it is insinuating that if you possess the PCM1 gene then you will have SZ. This means that this explanation is ignoring other factors such as psychological factors and family upbringing which could be more important in explaining SZ – for example it has been found that certain parenting styles (e.g. the schizophrenogenic mother) in an individuals childhood could trigger symptoms of SZ in adulthood.

Similarly, the diathesis stress model states that there is a genetic vulnerability in schizophrenia but this vulnerability is only likely to be triggered if there is a stress-trigger in the individual’s life. In other words, you may be born with a gene which makes you particularly vulnerable to SZ but if your life is relatively stress free, then you may not end up having the disorder at all. Thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ. Therefore taking a more holistic perspective in understanding the causes of SZ may lead to more effective treatments rather than just focusing on genes alone.

Question 11

What are neural correlates (schizophrenia)

Answer 11

Neural correlates are measurements of the structure or function of the brain that have a relationship with SZ especially different regions of the brain. Neural correlates also refers to how different neurotransmitters such as dopamine and serotonin (either excessive levels or low levels) in different parts of the brain can also play a part in SZ.

Question 12

Neural correlates - ventricles

Answer 12

Using brain-imaging techniques, researchers have discovered that many schizophrenics have enlarged ventricles, cavities in the brain that supply nutrients and remove waste – the ventricles of a person with SZ are on average about 15% bigger than normal (Torrey, 2002).

People with SZ who have enlarged ventricles tend to display more negative than positive symptoms. These people also tend to respond poorly to typical antipsychotic drugs. The enlarged ventricles may be the result of poor brain development or tissue damage, and these problems may lead to the development of SZ.

Question 13

Neural correlates - prefrontal cortex

Answer 13

The prefrontal cortex (PFC) is the main area of the brain involved in executive control (i.e. planning, reasoning and judgement) and research has shown that this is impaired in schizophrenic patients (Weinberger and Gallhofer, 1997).

Question 14

Neural correlates - hippocampus

Answer 14

The hippocampus is an area of the brain in the temporal lobe and several studies have reported anatomical changes in the hippocampus in schizophrenic patients (Conrad et al., 1991). Deficits in the nerve connections between the hippocampus and prefrontal cortex have found to correlate with the degree of memory impairments in schizophrenics.

Question 15

Strengths of neural correlates of schizophrenia

Answer 15

There is research evidence to support the structural changes in the brain between SZ and non SZ such as Torrey’s study with reference to enlarged brain ventricles and Conrad’s study with regards to the hippocampus.

Furthermore, this research evidence can be validated through brain scanning which is an objective method suggesting that there is face validity to the neural correlates explanation because one can actually observe the structural brain changes that occur with schizophrenic patients – this can then help to tailor make treatments that will reduce the symptoms of SZ.

Question 16

Weaknesses of neural correlates of schizophrenia

Answer 16

The problem with looking at different brain regions is the fact that there are individual differences in sufferers of schizophrenia and not all patients have deficits in the functioning of different brain regions.

Also as there are different brain regions involved in SZ, it may be difficult to pinpoint which brain region is causing the symptoms. Furthermore, it may be difficult to establish cause and effect in terms of neuroanatomy as evidence is correlational in other words, did the sufferer have abnormalities in a particular brain region and then contract schizophrenia or did the individual contract schizophrenia and then show brain abnormalities?

Question 17

What is dopamine

Answer 17

Dopamine is one of the brain’s neurotransmitters — a chemical that ferries information between neurons. Dopamine helps regulate movement, attention, learning, and emotional responses. It also enables us not only to see rewards, but to take action to move toward them.

Question 18

What are the two consequences of the dopamine hypothesis

Answer 18

Hyperdopaminergia and Hypodopaminergia

Question 18

What is the dopamine hypothesis

Answer 18

The dopamine hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of SZ. Thus messages from neurons that transmit dopamine fire too easily and often, leading to hallucinations and delusions.

Schizophrenics are thought to have particularly high levels of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing

Question 19

Hyperdopaminergia in the subcortex

Answer 19

This states that there are high levels of activity of dopamine in an area of the brain known as the subcortex (i.e. the central areas of the brain). For example an excess of dopamine receptors in the Broca’s area (which is responsible for speech production) may be associated with problems in speech and/or the experience of auditory hallucinations

Question 20

Hypodopaminergia in the cortex

Answer 20

Goldman-Rakic et al, (2004) have focused on the role of low levels of dopamine in the prefontal cortex (responsible for decision making and thinking) on negative symptoms of SZ.

It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia

Question 21

Strengths of the dopamine hypothesis for schizophrenia

Answer 21

There is evidence from drug research to support the Dopamine Hypothesis. With regards to the dopamine hypothesis, this neural correlates explanation is supported through drug research since dopamine agonists like amphetamines tend to increase dopamine levels and make the schizophrenic symptoms worse in sufferers and can produce schizophrenic-like symptoms in non-sufferers thus supporting this idea of Hyperdopaminergia.

Also, antipsychotic drugs act like antagonists – which act to reduce the levels of dopamine in schizophrenic patients (which thus help control the symptoms of SZ) supporting the idea that dopamine levels are high in SZ and can be reduced through drugs (e.g. Tauscher et al, 2014).

Furthermore, Lindstroem et al. (1999) have found that that chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics compared to controls again suggesting that schizophrenics produce more dopamine. Thus the abundance of evidence suggests that the dopamine hypothesis is definitely relevant in understanding schizophrenia

Question 22

Weaknesses of the dopamine hypothesis for schizophrenia

Answer 22

Problems with the dopamine hypothesis – the dopamine hypothesis could be criticised to being biological determinist which means an individual has no control over this whatsoever. However, the dopamine hypothesis alone cannot be seen as the sole cause of SZ since there are other biological and psychological factors that contribute such as upbringing in terms of family dysfunction or cognitive explanations which focus on impaired thinking which could definitely explain the hallucinations and delusions.

Also much more recent research has also focused on the attention of glutamate – another neurotransmitter that has been implicated in SZ (Moghadamm and Javitt, 2012) suggesting that dopamine might not be the only neurotransmitter responsible for SZ and other neurotransmitters may also be involved.

The Correlation-causation problem – as there are a number of neural correlates of SZ such as brain structure and neurotransmitters and although studies support neural correlates, there are some important questions that are left unanswered with such evidence. Most importantly, does high or low levels of dopamine cause SZ? There could be other explanations for the correlation.

For example, there is a correlation between high levels of dopamine and experiencing symptoms of SZ. However, did the individual start having excess levels of dopamine in that brain region and start experiencing symptoms of SZ or did the individual first experience symptoms of SZ and consequently have high levels of dopamine? This point poses a serious problem to the neural correlates explanation as it does not really explain the cause and effect