Key terms

Genetics - Genes consist of DNA strands. DNA produces ‘instructions’ for general physical features of an organism (such as eye colour, height) but also specific physical features (neurotransmitter levels and size of brain structures) These may impact on psychological features (such as intelligence and mental disorder) Genes are transmitted from parents to offspring.

Dopamine - A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure. Unusually high levels are associated with schizophrenia and unusually low levels are associated with Parkinson’s disease.

Neural correlates - Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience.

Biological explanations

The genetic basis of schizophrenia

Schizophrenia runs in families, weak evidence in itself for genetic link because family members tend to share aspects of their environment as well as many of their genes.

There is a strong relationship between the degree of genetic similarity and shared risk of schizophrenia - Gottesman

Candidate genes - individual genes are believed to be associated with the risk of inheritance. Because a number of genes each appear to confer a small increased risk of schizophrenia it appears that schizophrenia is polygenic. (it requires a number of factors to work in combination)

Because different studies have identified different candidate genes it also appears that schizophrenia is aetiologically heterogeneous (different combinations of factors can lead to the condition)

Ripke et al - carried out a huge study combining all previous data from genome-wide studies of schizophrenia. The genetic makeup of 37,000 people diagnosed with schizophrenia was compared to 113,000 controls.

108 genetic variations were associated with increased risk of schizophrenia. Genes associated with increased risk included those coding for the functioning of a number of neurotransmitters including dopamine.

The dopamine hypothesis

Neurotransmitters - the brain’s chemical messengers appear to work differently in the brain of a person with schizophrenia. Dopamine is important in the functioning of several brain systems that may be implicated in the symptoms of schizophrenia.

Hyperdopaminergia in the subcortex - focused on the possible role of high levels of activity of dopamine (hyperdopaminergia) in the subcortex i.e the central areas of the brain. For example. an excess of dopamine receptors in Broca’s area (which is responsible for speech production) may be associated with poverty of speech and/or the experience of auditory hallucinations.

Hypodopaminergic in the cortex - Goldman-Rakic et al (2004) have identified a role of flow levels of dopamine (hypodopaminergic) in the prefrontal cortex (responsible for thinking and decision making) in the negative symptoms of schizophrenia. It may be that both hyper and hyperdopaminergia are correct explanations- both high and low levels of dopamine in different regions are involved in schizophrenia.

Neural correlates of schizophrenia

Neural correlates are measurements of the structure or function of the brain that correlate with an experience. Both positive and negative symptoms have neural correlates for schizophrenia.

Neural correlates of negative symptoms

one negative symptom avolition involves the loss of motivation. Motivation involves the anticipation of a reward and certain regions of the brain for example ventral striatum are believed to be particularly involved in this anticipation. It therefore follows the abnormally of areas like the ventral striatum may be involved in the development of avolition. Juckel et al have measured activity levels in the ventral striatum in schizophrenia and found lower levels of activity than those observed in controls. Moreover, they observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms of schizophrenia.

Neural correlates of positive symptoms

Positive symptoms also have neural correlates. Allen et al (2007) scanned the brains of people experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs of others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group who also made more errors than the control group. We can thus say that reduced activity in these areas of the brain is a neural correlate of auditory hallucination.

Evaluation

• Multiple sources of evidence for genetic susceptibility

Gottesman (1991) study clearly shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies such as that by Pekka Tienari et al (2004) clearly show that children of people with schizophrenia are still at heightened risk of schizophrenia if adopted into families with no history of schizophrenia. There is also evidence from studies conducted at the molecular level showing that particular genetic variations significantly increase the risk of schizophrenia (Ripke et al)

• Mixed evidence of the dopamine hypothesis

Dopamine agonists like amphetamine that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia like symptoms in people not diagnosed with schizophrenia. (Curran et al) Antipsychotic drugs work by reducing dopamine activity (Tauscher et al 2014) Both kinds of drug study suggest an important role in schizophrenia. Radioactive labelling studies such as that by Lindstroem et al (1999) have found that chemicals needed to produce dopamine are taken up in faster in the brains of people with schizophrenia than controls, suggesting that they produce more dopamine.

There is also evidence to suggest that dopamine does not provide a complete explanation for schizophrenia. Some the of the genes identified in the Ripke et al study code for the production of other neurotransmitters, so it appears that dopamine is likely to be one important factor of schizophrenia so are the other neurotransmitters. Much of the attention in current research has shifted to the role of a neurotransmitter called glutamate (Moghaddam and Javitt 2012) Evidence for the dopamine hypothesis can perhaps be best described as mixed.

• Correlation-causation problem

There are a number of neural correlates of schizophrenia symptoms including both negative and positive.

For example, a correlation between levels of activity in the ventral striatum and negative symptoms of schizophrenia. It may be something wrong in the striatum that is causing negative symptoms however it is also possible that negative symptoms means that less information passes through striatum resulting in the reduced activity. A third possibility is that another factor influence both the negative symptoms and the ventral striatum activity. The existence of neural correlates in schizophrenia therefore tells us relatively little in itself.

• The role of mutation

Schizophrenia can take place in the absence of a family history of the disorder, one explanation for this mutation in parental DNA. This can be used by radiation, poison or viral infection. Evidence for the role of mutation comes from a study showing a positive correlation between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al 2002)

The increase from 0.7% to 2% with parental age does suggest a biological cause of schizophrenia. However, this is purely a correlation between mutation of aging paternal sperm and schizophrenia, suggesting a relationship between these two factors rather than one causing the other.

• The role of the psychological environment is important but unclear.

Other evidence to suggest an important role for environmental factors, including psychological ones such as family functioning during childhood. After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%.

Identical (MZ) twins share 100% of genes but concordance rates for schizophrenia are around 50%. If the disorder was caused purely by genetic factors then this percentage should be 100%. As it is not this indicates that genes and therefore biology are only partly responsible and thus environmental / psychological factors must play some role.