Biological Explanations Of SZ

Question 1

What are the two factors the biological explanations are based on:

Answer 1

The genetic basis
The neural basis correlates including the dopamine hypothesis

Question 2

What’s the genetic basis about (short)

Answer 2

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

Question 3

AO1 points - family studies

Answer 3

• determines if SZ ppls relatives are more similarly affected than non relatives
• both parents have SZ, then offspring = 46% chance
• one parent has SZ, offspring = 13% chance
• sibling has SZ’ 9% chance

Question 4

What do twin studies investigate (AO1 points)

Answer 4

• can check nature / nurture debate of contributions on sz
• The more genetically similar you are, more likely to get MZ:
  MZ (100% identical twins) = 48% concordance rate
  DZ (50% identical twins) = 17% concordance rate

Question 5

Adoption studies AO1 points

Answer 5

• to see influence of nature and nurture when away from SZ parents etc
  Tienari et al study showed only a small link between genes and SZ

Question 6

What did Tienari et al do?

Answer 6

Finland study
164 adoptees who’s biological mothers had been diagnosed with SZ, 11 (6.7%) diagnosed with SZ

Control group - of 197 adoptees (adopted by ppl that were not schizophrenic), only 4 (2%) were diagnosed with SZ

Question 7

Candidate gene associated with SZ

Answer 7

PCM1

Question 8

But is sz considered monogenic or polygenic

Answer 8

Polygenic

Question 9

Evidence using family studies found what chromosome to be associated with SZ

Answer 9

Chromosome 8p21-22

Question 10

What other gene variants can create susceptibility to developing SZ

Answer 10

NRG1
NRG3
ERBB4

Question 11

Genetic makeup of […] SZ patients worldwide compared with […] controls to find […] separate genetic variations associated with an increased risk

Answer 11

37000
113000 controls
108 genes

Question 12

(+) of genetic basis = the wealth of evidence e.g.

Answer 12

Tienari’s study and also:
Joseph’s review of twin studies that were carried out up to 2001 and found an overall concordance rate for MZ twins as 40% but DZ was 7.4% (concordance pretty high for MZ so supports role of genes)

Question 13

(-) of genetic basis: why are adoption studies not as legit?

Answer 13

Nature vs nurture hard to investigate, as we can’t tell which one is affecting it
Even attempting to look at children adopted, they’re usually taken in by relatives with similar parenting styles so not always good comparisons for the effects of nature vs nurture

Question 14

(-) how is the genetic explanation biologically reductionist

Answer 14

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.

Question 15

(-) how does the diathesis stress model go against the genetic vulnerability

Answer 15

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 16

What are neural correlates

Answer 16

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 17

Examples of brain regions that have associations with SZ (U don’t need 2 know this?)

Answer 17

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.

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).

Also, 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 18

AO3 of the brain regions neural correlates research

Answer 18

Strengths

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.

Weaknesses

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 19

Whats the most researched example of neural correlates

Answer 19

Dopamine neurotransmitter
(Bc the dopamine hypothesis)

Question 20

What’s dopamine

Answer 20

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. Since dopamine contributes to feelings of pleasures and satisfaction as part of the reward system, the neurotransmitter also plays a part in addiction.

Question 21

What does the dopamine hypothesis claim

Answer 21

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 22

The 2 consequences of the dopamine hypothesis

Answer 22

Hyperdopaminergia
Hypodopaminergia

Question 23

Where does hyperdopaminergia occur

Answer 23

In the subcortex

Question 24

What’s hyperdopaminergia

Answer 24

this is based on the original version of the dopamine hypothesis in explaining SZ – 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 25

What’s hypodopaminergia & where does it happen

Answer 25

In the cortex

recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex. 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.

Question 26

(+) of the dopamine hypothesis? (Drug evidence)

Answer 26

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 27

(-) weaknesses of the dopamine hypothesis e.g. determinist + not complete explanation + other neurotransmitters?

Answer 27

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.
Could also be due to neural correlates of SZ like brain structure

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.

Although studies support it, could be correlation not causation