You need to be able to describe, evaluate and compare TWO biological explanations of schizophrenia. One of them MUST be the functioning of neurotransmitters (the "Dopamine Hypothesis"), so you need to know this in detail and the Exam could ask your specifically about neurotransmitters. The Specification also mentions genes and mental health, so the second explanation here is a genetic one. You could be asked for "a biological explanation of schizophrenia OTHER THAN NEUROTRANSMITTERS" or "how genes affect mental health" (with specifying schizophrenia).
|
BIOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA
The Unit 2 Exam expects you to know about two biological explanations of schizophrenia: the functions of neurotransmitters and one other.
You are also expected to understand a biological treatment for schizophrenia which is linked to these explanations. As part of Unit 1's Biological Approach, you will have looked at a twin study (Gottesman & Shields) and an adoption study (Kety et al.) which both claim that there is a genetic aspect to schizophrenia and that the disorder is passed on, biologically, in families.
|
SCHIZOPHRENIA & THE FUNCTIONS OF NEUROTRANSMITTERS
|
Neurotransmitters are "fast chemical messengers" that travel between neurons (brain cells) by crossing the synapse. They bind themselves to receptors on the next neuron and pass in their message in the form of a small electric charge.
Dopamine is an important neurotransmitter that regulates mood and attention. It seems to be linked to schizophrenia in a number of ways. The Dopamine Hypothesis was proposed by Arvid Carlsson and suggests that schizophrenia is caused by too much dopamine - or too many dopamine receptors - in key areas of the brain. |
Dopamine systems in the mesolimbic pathway may contribute to the positive symptoms of schizophrenia (such as hallucinations).
Dopamine function in the mesocortical pathway may be responsible for the negative symptoms, such as avolition (lack of motivation) and alogia (inability to speak).
Dopamine function in the mesocortical pathway may be responsible for the negative symptoms, such as avolition (lack of motivation) and alogia (inability to speak).
L-dopa is a drug used to treat Parkinson’s disease by boosting dopamine levels in the brain. Carlsson discovered that giving L-Dopa to animals reduced their Parkinsons-like symptoms; L-dopa also reduced Parkinsons symptoms in humans but gave them psychotic symptoms that were similar to schizophrenia.
Amphetamine is a recreational drug which increases dopamine activity and produces schizophrenia-like symptoms in users (known as 'cocaine psychosis'). Drugs like LSD, which are known to increase dopamine activity, also trigger schizophrenic symptoms in healthy people and exaggerate the positive symptoms of those with the disorder.
Antipsychotic drugs like phenothiazines (PTZ) reduce the symptoms of schizophrenia and work by blocking dopamine receptors.
Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).
Amphetamine is a recreational drug which increases dopamine activity and produces schizophrenia-like symptoms in users (known as 'cocaine psychosis'). Drugs like LSD, which are known to increase dopamine activity, also trigger schizophrenic symptoms in healthy people and exaggerate the positive symptoms of those with the disorder.
Antipsychotic drugs like phenothiazines (PTZ) reduce the symptoms of schizophrenia and work by blocking dopamine receptors.
Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).
The contemporary study into schizophrenia by Carlsson et al. (1999) introduces a different explanation based on neurotransmitters: the Glutamate Hypothesis
SCHIZOPHRENIA & GENETICS
|
Pinpointing the exact genes responsible has not been easy: schizophrenia seems to involve several genes rather than just one. However, a recent study has narrowed down this search.
Sekar et al. (2016) analysed 100,000 human DNA samples from 30 different countries. They identified a gene called complement component 4 (C4), which is part of the immune system. Genetic analysis of 65,000 people found that those who had particular forms of the C4 gene showed higher risk of developing schizophrenia. |
Short introduction to the C4 gene
|
The human brain normally undergoes synapse pruning during adolescence. This is normally a good thing because it's part of learning: the brain 'prunes' under-used or damaged connections to make space for new ones (this is an example of "use it or lose it" going on in the brain). C4 plays a role in pruning synapses but excessive pruning could lead to the symptoms seen in schizophrenia. Test mice with increased levels of C4 activity lost more brain cells as they matured.
This would explain why schizophrenia symptoms appear after adolescence and why the brains of people with schizophrenia have a thinner cerebral cortex with fewer synapses than healthy brains.
This would explain why schizophrenia symptoms appear after adolescence and why the brains of people with schizophrenia have a thinner cerebral cortex with fewer synapses than healthy brains.
The main role of C4 is to "mark" infections so that they are attacked by the immune system. It seems as if, when it is over-active, C4 actually damages the brain it is meant to protect.
APPLYING BIOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA
|
EVALUATING BIOLOGICAL EXPLANATIONS
|
A "black box" is one of those indestructible machines on an aeroplane that records all the flight details and can survive a crash or explosion. Getting into a black box is very difficult but, if you do, it contains the information about what really happened to the plane.
Pub quiz trivia: black boxes are actually orange. |
When you put the genetic explanation together with the dopamine hypothesis, you approach a complete picture of what causes schizophrenia. There are still missing pieces in the puzzle (what's the link between synaptic pruning and neurotransmitter activity?) but the two explanations are COMPLEMENTARY - they work together.
The contemporary study into schizophrenia by Carlsson et al. (1999) suggests a different explanation: the Glutamate Hypothesis. Glutamate is another neurotransmitter linked to attention and memory. Schizophrenia symptoms seem to be linked to low levels of glutamate - perhaps because glutamate regulates dopamine, so when glutamate is blocked, dopamine levels become abnormal.
Applications
Biological explanations have led to the development of antipsychotic drugs. However, these drugs are much more effective at reducing positive symptoms than negative symptoms. They also have nasty side-effects: lethargy (extreme sleepiness), weight gain, sexual problems and a high risk of diabetes.
Critics in the Recovery Movement reject the biological explanation and the dependency on drugs, which they argue do more harm than good and only create profits for "Big Pharma" (the medical drugs industry). The recovery model recommends that people with schizophrenia stop thinking of themselves as 'sick', embrace their symptoms and learn to cope with them and focus on changing their lifestyle/outlook instead.
Critics in the Recovery Movement reject the biological explanation and the dependency on drugs, which they argue do more harm than good and only create profits for "Big Pharma" (the medical drugs industry). The recovery model recommends that people with schizophrenia stop thinking of themselves as 'sick', embrace their symptoms and learn to cope with them and focus on changing their lifestyle/outlook instead.
EXEMPLAR ESSAY
|